Displaying publications 1 - 20 of 32 in total

Abstract:
Sort:
  1. Al-Joudi FS, Iskandar ZA, Imran AK
    Med J Malaysia, 2007 Mar;62(1):6-8.
    PMID: 17682561 MyJurnal
    Survivin is a 16.5-kDa intracellular protein also known as AP14 or BIRC5. It inhibits apoptosis and regulates cell division and belongs to the inhibitors of apoptosis (IAP) gene family. In the majority of neoplasms investigated for survivin expression, high levels of the IAP proteins were predictive of tumour progression, either in terms of disease-free survival or overall survival, thus providing significant prognostic information. Hence, the prognostic value of survivin expression in tumour masses of invasive ductal carcinoma has been investigated. It was found that negative and low expression of survivin correlated significantly with favourable outcomes. Conversely, high expression correlated with unfavourable outcomes. The five-year survival rate was higher among the cases with low and negative survivin expression, compared to those with higher survivin expression. However, this correlation was found to be insignificant statistically. Furthermore, a statistical model has been devised to explain the combined effects of survivin expression and its sub-cellular localisation, p-53 expression and lymph nodal involvement, on the outcomes of these patients.
    Matched MeSH terms: Breast Neoplasms/physiopathology*
  2. Suzana S, Cham BG, Ahmad Rohi G, Mohd Rizal R, Fairulnizal MN, Normah H, et al.
    Singapore Med J, 2009 Mar;50(3):265-9.
    PMID: 19352569
    The purpose of this study was to assess the relationship between selenium status and intake among breast cancer patients from the Klang Valley.
    Matched MeSH terms: Breast Neoplasms/physiopathology
  3. Gao Y, Zhang W, Liu C, Li G
    Sci Rep, 2019 12 11;9(1):18844.
    PMID: 31827114 DOI: 10.1038/s41598-019-54289-6
    Resistance to tamoxifen is a major clinical challenge. Research in recent years has identified epigenetic changes as mediated by dysregulated miRNAs that can possibly play a role in resistance to tamoxifen in breast cancer patients expressing estrogen receptor (ER). We report here elevated levels of EMT markers (vimentin and ZEB1/2) and reduced levels of EMT-regulating miR-200 (miR-200b and miR-200c) in ER-positive breast cancer cells, MCF-7, that were resistant to tamoxifen, in contrast with the naïve parental MCF-7 cells that were sensitive to tamoxifen. Further, we established regulation of c-MYB by miR-200 in our experimental model. C-MYB was up-regulated in tamoxifen resistant cells and its silencing significantly decreased resistance to tamoxifen and the EMT markers. Forced over-expression of miR-200b/c reduced c-MYB whereas reduced expression of miR-200b/c resulted in increased c-MYB We further confirmed the results in other ER-positive breast cancer cells T47D cells where forced over-expression of c-MYB resulted in induction of EMT and significantly increased resistance to tamoxifen. Thus, we identify a novel mechanism of tamoxifen resistance in breast tumor microenvironment that involves miR-200-MYB signaling.
    Matched MeSH terms: Breast Neoplasms/physiopathology
  4. Pandey M, Thomas BC, Ramdas K, Eremenco S, Nair MK
    Qual Life Res, 2002 Mar;11(2):87-90.
    PMID: 12018741
    BACKGROUND: Recent advances in diagnosis and treatment of cancer have led to an increase in cancer survival, and hence, there is a greater emphasis on quality beside quantity of survival. Developing countries too have begun to recognize the need for monitoring quality of life (QOL). However, in most of the developing countries, a validated and reliable tool for the purpose is yet to be realized.

    MATERIAL AND METHOD: The functional assessment of chronic illness therapy (FACIT) system is a collection of QOL questionnaires targeted to measure QOL in chronic illness. The functional assessment of cancer therapy for breast cancer (FACT-B) was translated into the local language (Malayalam) and tested for validity and reliability.

    RESULTS: The tool thus developed showed substantial sensitivity, as does the source tool. The Cronbach's alpha for the total FACT-B was 0.87, which is similar to the alpha of 0.9 observed in the FACT-B English version. The mean FACT-B score was 94.3 compared to 112.8 for the source tool.

    CONCLUSION: The Malayalam translation of the FACT-B questionnaire was developed, tested and validated, and was found satisfactory in comparison to the source tool.

    Matched MeSH terms: Breast Neoplasms/physiopathology*
  5. Ismail NZ, Adebayo IA, Mohamed WAS, Mohamad Zain NN, Arsad H
    Mol Biol Rep, 2021 Nov;48(11):7361-7370.
    PMID: 34665399 DOI: 10.1007/s11033-021-06743-w
    BACKGROUND: C. vespertiliomis extracts were evaluated for antiproliferative and apoptosis effect on breast cancer (MCF7) cells.

    METHODS AND RESULTS: The leaves extracts were analysed for its antiproliferative effect on breast cancer (MCF7) cells and normal epithelial breast (MCF 10A) cells using Sulforhodamine B (SRB) assay. The selective extract was evaluated for its ability to induce apoptosis using Annexin V-FITC apoptosis staining and the expression of molecular genes using qualitative reverse transcription-polymerase chain reaction (RT-PCR) against MCF7 cells. Gas chromatography-mass spectrometry (GC-MS) was used to identify the compounds from the selective extract. The findings showed that dichloromethane fraction (CV-Dcm) extract had high antiproliferative effect against MCF7 cells (IC50 = 24 µg/mL, selective index (SI) = 8.17). The percentages of apoptosis cells in CV-Dcm-treated MCF7 cells was 58.8%. The CV-Dcm extract induced downregulation of PCNA level. The apoptotic genes were also triggered in both extrinsic and intrinsic signaling pathways, affecting a 1.5-fold increase in BAX, 1.4-fold increase in cytochrome c, 1.3-fold increase in caspase-8, 1.7-fold increase in caspase-3 and 0.5-fold-decrease in BCL-2. Treated MCF7 cells also activated P53-dependent apoptotic death pathway.

    CONCLUSIONS: The present work strongly suggests that high efficacy of CV-Dcm extract was attributed to its antiproliferative and apoptosis-inducing activation in MCF7 cells, most likely due to its favourable compounds.

    Matched MeSH terms: Breast Neoplasms/physiopathology
  6. Ng KH, Lau S
    Med Phys, 2015 Dec;42(12):7059-77.
    PMID: 26632060 DOI: 10.1118/1.4935141
    Breast density is a strong predictor of the failure of mammography screening to detect breast cancer and is a strong predictor of the risk of developing breast cancer. The many imaging options that are now available for imaging dense breasts show great promise, but there is still the question of determining which women are "dense" and what imaging modality is suitable for individual women. To date, mammographic breast density has been classified according to the Breast Imaging-Reporting and Data System (BI-RADS) categories from visual assessment, but this is known to be very subjective. Despite many research reports, the authors believe there has been a lack of physics-led and evidence-based arguments about what breast density actually is, how it should be measured, and how it should be used. In this paper, the authors attempt to start correcting this situation by reviewing the history of breast density research and the debates generated by the advocacy movement. The authors review the development of breast density estimation from pattern analysis to area-based analysis, and the current automated volumetric breast density (VBD) analysis. This is followed by a discussion on seeking the ground truth of VBD and mapping volumetric methods to BI-RADS density categories. The authors expect great improvement in VBD measurements that will satisfy the needs of radiologists, epidemiologists, surgeons, and physicists. The authors believe that they are now witnessing a paradigm shift toward personalized breast screening, which is going to see many more cancers being detected early, with the use of automated density measurement tools as an important component.
    Matched MeSH terms: Breast Neoplasms/physiopathology
  7. Lua PL, Salihah NZ, Mazlan N
    Malays J Nutr, 2012 Aug;18(2):173-84.
    PMID: 24575665 MyJurnal
    Nutritional decline is typically accepted as a consequent of the course of treatment for cancer. This study aimed to (1) assess body weight status and dietary intake of breast cancer patients on chemotherapy and (2) to correlate Body Mass Index (BMI), energy and protein intake with health-related quality of life (HRQoL) profile.
    Matched MeSH terms: Breast Neoplasms/physiopathology*
  8. Majid HA, Keow LP, Islam T, Su TT, Cantwell M, Taib NA, et al.
    J Acad Nutr Diet, 2018 04;118(4):705-713.
    PMID: 28756991 DOI: 10.1016/j.jand.2017.05.024
    BACKGROUND: Lifestyle factors, such as diet, body weight, and physical activity, are linked to better survival after breast cancer (BC) diagnosis. A high percentage of the Malaysian population is overweight or obese. In addition, studies have shown a disparity in survival among Malaysian women compared with other higher-income countries. The Malaysian Breast Cancer Survivorship Cohort (MyBCC) study aims to study lifestyle factors that affect survival in BC survivors. These are the preliminary findings on the nutritional status of Malaysian BC survivors.

    OBJECTIVE: Our aim was to evaluate the nutritional status of BC survivors at 1 year after diagnosis.

    DESIGN: This was a cross-sectional study of 194 participants from the MyBCC study, recruited within 1 year of their diagnosis. Participants completed a 3-day food diary.

    PARTICIPANTS: Malaysian women (aged 18 years and older) who were newly diagnosed with primary BC, managed at the University Malaya Medical Center, and able to converse either in Malay, English, or Mandarin were included.

    MAIN OUTCOME MEASURES: Dietary intake and prevalence of overweight or obesity among participants 1 year after diagnosis were measured.

    STATISTICAL ANALYSES PERFORMED: Student's t test and analysis of variance or its equivalent nonparametric test were used for association in continuous variables.

    RESULTS: About 66% (n=129) of participants were overweight or obese and >45% (n=86) had high body fat percentage 1 year after diagnosis. The participants' diets were low in fiber (median=8.7 g/day; interquartile range=7.2 g/day) and calcium (median=458 mg/day; interquartile range=252 mg/day). Ethnicity and educational attainment contributed to the differences in dietary intake among participants. Higher saturated fat and lower fiber intake were observed among Malay participants compared with other ethnic groups.

    CONCLUSIONS: Overweight and obesity were highly prevalent among BC survivors and suboptimal dietary intake was observed. Provision of an individualized medical nutrition therapy by a qualified dietitian is crucial as part of comprehensive BC survivorship care.

    Matched MeSH terms: Breast Neoplasms/physiopathology*
  9. Chan EWC, Soon CY, Tan JBL, Wong SK, Hui YW
    J Integr Med, 2019 May;17(3):155-160.
    PMID: 30928277 DOI: 10.1016/j.joim.2019.03.003
    Ursolic acid (UA) is a pentacyclic triterpene of the ursane type. As a common chemical constituent among species of the family Lamiaceae, UA possesses a broad spectrum of pharmacological properties. This overview focuses on the anticancer properties of UA against breast cancer (BC) and colorectal cancer (CRC) that are most common among women and men, respectively. In vitro studies have shown that UA inhibited the growth of BC and CRC cell lines through various molecular targets and signaling pathways. There are several in vivo studies on the cytotoxic activity of UA against BC and CRC. UA also inhibits the growth of other types of cancer. Studies on structural modifications of UA have shown that the -OH groups at C3 and at C28 are critical factors influencing the cytotoxic activity of UA and its derivatives. Some needs for future research are suggested. Sources of information were from ScienceDirect, Google Scholar and PubMed.
    Matched MeSH terms: Breast Neoplasms/physiopathology
  10. Chong ZX, Yeap SK, Ho WY
    J Biomed Sci, 2021 Mar 25;28(1):21.
    PMID: 33761957 DOI: 10.1186/s12929-021-00715-9
    Breast cancer is the most common solid cancer that affects female population globally. MicroRNAs (miRNAs) are short non-coding RNAs that can regulate post-transcriptional modification of multiple downstream genes. Autophagy is a conserved cellular catabolic activity that aims to provide nutrients and degrade un-usable macromolecules in mammalian cells. A number of in vitro, in vivo and clinical studies have reported that some miRNAs could modulate autophagy activity in human breast cancer cells, and these would influence human breast cancer progression and treatment response. Therefore, this review was aimed to discuss the roles of autophagy-regulating miRNAs in influencing breast cancer development and treatment response. The review would first introduce autophagy types and process, followed by the discussion of the roles of different miRNAs in modulating autophagy in human breast cancer, and to explore how would this miRNA-autophagy regulatory process affect the disease progression or treatment response. Lastly, the potential applications and challenges of utilizing autophagy-regulating miRNAs as breast cancer biomarkers and novel therapeutic agents would be discussed.
    Matched MeSH terms: Breast Neoplasms/physiopathology*
  11. Kumar DH, Kutty MK
    Indian J Pathol Microbiol, 2012 Apr-Jun;55(2):147-53.
    PMID: 22771633 DOI: 10.4103/0377-4929.97842
    Cancer is fundamentally a cellular genetic disease capable of transferring the "disease" to the next generation of mutated cells. Similar proliferative and information transferring capacity exists in the stem cells of various organ systems in the human body. Understanding the bio-mechanism of stem cell metabolism and its regulation by signaling molecules and extracellular micro-environment is an important step toward successful prevention and treatment of cancer. According to the cancer stem cell hypothesis, both hereditary and sporadic cancers can arise from deregulation of these cancer stem cells (CSCs), triggered by genetic and environmental factors. It is shown that deregulation of normal self-renewal pathways in undifferentiated breast stem cells or progenitor cells had altered mammary system or progenitor cells, resulting in abnormally differentiated cells in human and rodent breast cancer cell lines. Breakthroughs in molecular pathways have important therapeutic implications. Hence, significant stress is laid on targeting signaling molecules and their micromilieu in breast cancer therapy.
    Matched MeSH terms: Breast Neoplasms/physiopathology*
  12. Pfister NT, Fomin V, Regunath K, Zhou JY, Zhou W, Silwal-Pandit L, et al.
    Genes Dev., 2015 Jun 15;29(12):1298-315.
    PMID: 26080815 DOI: 10.1101/gad.263202.115
    Mutant p53 impacts the expression of numerous genes at the level of transcription to mediate oncogenesis. We identified vascular endothelial growth factor receptor 2 (VEGFR2), the primary functional VEGF receptor that mediates endothelial cell vascularization, as a mutant p53 transcriptional target in multiple breast cancer cell lines. Up-regulation of VEGFR2 mediates the role of mutant p53 in increasing cellular growth in two-dimensional (2D) and three-dimensional (3D) culture conditions. Mutant p53 binds near the VEGFR2 promoter transcriptional start site and plays a role in maintaining an open conformation at that location. Relatedly, mutant p53 interacts with the SWI/SNF complex, which is required for remodeling the VEGFR2 promoter. By both querying individual genes regulated by mutant p53 and performing RNA sequencing, the results indicate that >40% of all mutant p53-regulated gene expression is mediated by SWI/SNF. We surmise that mutant p53 impacts transcription of VEGFR2 as well as myriad other genes by promoter remodeling through interaction with and likely regulation of the SWI/SNF chromatin remodeling complex. Therefore, not only might mutant p53-expressing tumors be susceptible to anti VEGF therapies, impacting SWI/SNF tumor suppressor function in mutant p53 tumors may also have therapeutic potential.
    Matched MeSH terms: Breast Neoplasms/physiopathology*
  13. Love RR, Hossain SM, Hussain MM, Mostafa MG, Laudico AV, Siguan SS, et al.
    Eur J Cancer, 2016 06;60:107-16.
    PMID: 27107325 DOI: 10.1016/j.ejca.2016.03.011
    PURPOSE: In premenopausal women with metastatic hormone receptor-positive breast cancer, hormonal therapy is the first-line therapy. Gonadotropin-releasing hormone analogue + tamoxifen therapies have been found to be more effective. The pattern of recurrence risk over time after primary surgery suggests that peri-operative factors impact recurrence. Secondary analyses of an adjuvant trial suggested that the luteal phase timing of surgical oophorectomy in the menstrual cycle simultaneous with primary breast surgery favourably influenced long-term outcomes.

    METHODS: Two hundred forty-nine premenopausal women with incurable or metastatic hormone receptor-positive breast cancer entered a trial in which they were randomised to historical mid-luteal or mid-follicular phase surgical oophorectomy followed by oral tamoxifen treatment. Kaplan-Meier methods, the log-rank test, and multivariable Cox regression models were used to assess overall and progression-free survival (PFS) in the two randomised groups and by hormone-confirmed menstrual cycle phase.

    RESULTS: Overall survival (OS) and PFS were not demonstrated to be different in the two randomised groups. In a secondary analysis, OS appeared worse in luteal phase surgery patients with progesterone levels <2 ng/ml (anovulatory patients; adjusted hazard ratio 1.46, 95% confidence interval [CI]: 0.89-2.41, p = 0.14) compared with those in luteal phase with progesterone level of 2 ng/ml or higher. Median OS was 2 years (95% CI: 1.7-2.3) and OS at 4 years was 26%.

    CONCLUSIONS: The history-based timing of surgical oophorectomy in the menstrual cycle did not influence outcomes in this trial of metastatic patients. ClinicalTrials.gov number NCT00293540.

    Study site: Bangladesh, The Philippines, China, Nigeria,
    Indonesia, Malaysia, Taiwan, Morocco, and Vietnam
    Matched MeSH terms: Breast Neoplasms/physiopathology
  14. Nwanaji-Enwerem JC, Chung FF, Van der Laan L, Novoloaca A, Cuenin C, Johansson H, et al.
    Clin Epigenetics, 2021 12 17;13(1):224.
    PMID: 34920739 DOI: 10.1186/s13148-021-01218-y
    Metformin and weight loss relationships with epigenetic age measures-biological aging biomarkers-remain understudied. We performed a post-hoc analysis of a randomized controlled trial among overweight/obese breast cancer survivors (N = 192) assigned to metformin, placebo, weight loss with metformin, or weight loss with placebo interventions for 6 months. Epigenetic age was correlated with chronological age (r = 0.20-0.86; P 
    Matched MeSH terms: Breast Neoplasms/physiopathology*
  15. Subramaniyan V, Fuloria S, Gupta G, Kumar DH, Sekar M, Sathasivam KV, et al.
    Chem Biol Interact, 2022 Jan 05;351:109735.
    PMID: 34742684 DOI: 10.1016/j.cbi.2021.109735
    Epithelial growth factor receptor (EGFR) is a cell surface transmembrane receptor that mediates the tyrosine signaling pathway to carry the extracellular messages inside the cell and thereby alter the function of nucleus. This leads to the generation of various protein products to up or downregulate the cellular function. It is encoded by cell erythroblastosis virus oncogene B1, so called C-erb B1/ERBB2/HER-2 gene that acts as a proto-oncogene. It belongs to the HER-2 receptor-family in breast cancer and responds best with anti-Herceptin therapy (anti-tyrosine kinase monoclonal antibody). HER-2 positive breast cancer patient exhibits worse prognosis without Herceptin therapy. Similar incidence and prognosis are reported in other epithelial neoplasms like EGFR + lung non-small cell carcinoma and glioblastoma (grade IV brain glial tumor). Present study highlights the role and connectivity of EGF with various cancers via signaling pathways, cell surface receptors mechanism, macromolecules, mitochondrial genes and neoplasm. Present study describes the EGFR associated gene expression profiling (in breast cancer and NSCLC), relation between mitrochondrial genes and carcinoma, and several in vitro and in vivo models to screen the synergistic effect of various combination treatments. According to this study, although clinical studies including targeted treatments, immunotherapies, radiotherapy, TKi-EGFR combined targeted therapy have been carried out to investigate the synergism of combination therapy; however still there is a gap to apply the scenarios of experimental and clinical studies for further developments. This review will give an idea about the transition from experimental to most advanced clinical studies with different combination drug strategies to treat cancer.
    Matched MeSH terms: Breast Neoplasms/physiopathology*
  16. Srinivasan V, Spence DW, Pandi-Perumal SR, Trakht I, Esquifino AI, Cardinali DP, et al.
    Breast Cancer Res Treat, 2008 Apr;108(3):339-50.
    PMID: 17541739
    Although many factors have been suggested as causes for breast cancer, the increased incidence of the disease seen in women working in night shifts led to the hypothesis that the suppression of melatonin by light or melatonin deficiency plays a major role in cancer development. Studies on the 7,12-dimethylbenz[a]anthracene and N-methyl-N-nitrosourea experimental models of human breast cancer indicate that melatonin is effective in reducing cancer development. In vitro studies in MCF-7 human breast cancer cell line have shown that melatonin exerts its anticarcinogenic actions through a variety of mechanisms, and that it is most effective in estrogen receptor (ER) alpha-positive breast cancer cells. Melatonin suppresses ER gene, modulates several estrogen dependent regulatory proteins and pro-oncogenes, inhibits cell proliferation, and impairs the metastatic capacity of MCF-7 human breast cancer cells. The anticarcinogenic action on MCF-7 cells has been demonstrated at the physiological concentrations of melatonin attained at night, suggesting thereby that melatonin acts like an endogenous antiestrogen. Melatonin also decreases the formation of estrogens from androgens via aromatase inhibition. Circulating melatonin levels are abnormally low in ER-positive breast cancer patients thereby supporting the melatonin hypothesis for breast cancer in shift working women. It has been postulated that enhanced endogenous melatonin secretion is responsible for the beneficial effects of meditation as a form of psychosocial intervention that helps breast cancer patients.
    Matched MeSH terms: Breast Neoplasms/physiopathology*
  17. Koh CH, Bhoo-Pathy N, Ng KL, Jabir RS, Tan GH, See MH, et al.
    Br. J. Cancer, 2015 Jun 30;113(1):150-8.
    PMID: 26022929 DOI: 10.1038/bjc.2015.183
    Peripheral blood-derived inflammation-based scores such as the neutrophil-lymphocyte ratio (NLR) and platelet-lymphocyte ratio (PLR) have recently been proposed as prognostic markers in solid tumours. Although evidence to support these markers as unfavourable prognostic factors is more compelling in gastrointestinal cancers, very little is known of their impact on breast cancer. We investigated the association between the NLR and PLR, and overall survival after breast cancer.
    Matched MeSH terms: Breast Neoplasms/physiopathology*
  18. Ahmad U, Ahmed I, Keong YY, Abd Manan N, Othman F
    Biomed Res Int, 2015;2015:127828.
    PMID: 25821783 DOI: 10.1155/2015/127828
    Breast cancer is the malignant tumour that developed from cells of the breast and is the first leading cause of cancer death among women worldwide. Surgery, radiotherapy, and chemotherapy are the available treatments for breast cancer, but these were reported to have side effects. Newcastle disease virus (NDV) known as Avian paramyxovirus type-1 (APMV1) belongs to the genus Avulavirus in a family Paramyxoviridae. NDV is shown to be a promising anticancer agent, killing tumour cells while sparing normal cells unharmed. In this study, the oncolytic and cytotoxic activities of NDV AF2240 strain were evaluated on MDA-MB-231, human mammary carcinoma cell line, using MTT assay, and its inhibitory effects were further studied using proliferation and migration assays. Morphological and apoptotic-inducing effects of NDV on MD-MB-231 cells were observed using phase contrast and fluorescence microscopes. Detection of DNA fragmentation was done following terminal deoxyribonucleotide transferase-mediated Br-dUTP nick end labeling staining (TUNEL) assay, which confirmed that the mode of death was through apoptosis and was quantified by flow cytometry. Furthermore, analysis of cellular DNA content demonstrated that the virus caused an increase in the sub-G1 phase (apoptotic peak) of the cell cycle. It appears that NDV AF2240 strain is a potent anticancer agent that induced apoptosis in time-dependent manner.
    Matched MeSH terms: Breast Neoplasms/physiopathology*
  19. Tang EL, Rajarajeswaran J, Fung SY, Kanthimathi MS
    PMID: 24517259 DOI: 10.1186/1472-6882-13-347
    Coriandrum sativum is a popular culinary and medicinal herb of the Apiaceae family. Health promoting properties of this herb have been reported in pharmacognostical, phytochemical and pharmacological studies. However, studies on C. sativum have always focused on the aerial parts of the herb and scientific investigation on the root is limited. The aim of this research was to investigate the antioxidant and anticancer activities of C. sativum root, leaf and stem, including its effect on cancer cell migration, and its protection against DNA damage, with special focus on the roots.
    Matched MeSH terms: Breast Neoplasms/physiopathology*
  20. Reddy AS, Abd Malek SN, Ibrahim H, Sim KS
    BMC Complement Altern Med, 2013 Nov 12;13:314.
    PMID: 24215354 DOI: 10.1186/1472-6882-13-314
    BACKGROUND: Alpinia scabra, locally known as 'Lengkuas raya', is an aromatic, perennial and rhizomatous herb from the family Zingiberaceae. It is a wild species which grows largely on mountains at moderate elevations in Peninsular Malaysia, but it can also survive in the lowlands like in the states of Terengganu and Northern Johor. The present study reports the cytotoxic potential of A. scabra extracts from different parts of the plant.

    METHODS: The experimental approach in the present study was based on a bioassay-guided fractionation. The crude methanol and fractionated extracts (hexane, chloroform and water) from different parts of A. scabra (leaves, rhizomes, roots and pseudo stems) were prepared prior to the cytotoxicity evaluation against human ovarian (SKOV-3) and hormone-dependent breast (MCF7) carcinoma cells. The identified cytotoxic extracts were then subjected to chemical investigations in order to identify the active ingredients. A normal human lung fibroblast cell line (MRC-5) was used to determine the specificity for cancerous cells. The cytotoxic extracts and fractions were also subjected to morphological assessment, DNA fragmentation analysis and DAPI nuclear staining.

    RESULTS: The leaf (hexane and chloroform) and rhizome (chloroform) extracts showed high inhibitory effect against the tested cells. Ten fractions (LC1-LC10) were yielded after purification of the leaf chloroform extract. Fraction LC4 which showed excellent cytotoxic activity was further purified and resulted in 17 sub-fractions (VLC1-VLC17). Sub-fraction VLC9 showed excellent cytotoxicity against MCF7 and SKOV-3 cells but not toxic against normal MRC-5 cells. Meanwhile, eighteen fractions (RC1-RC18) were obtained after purification of the rhizome chloroform extract, of which fraction RC5 showed cytotoxicity against SKOV-3 cells with high selectivity index. There were marked morphological changes when observed using phase-contrast inverted microscope, DAPI nuclear staining and also DNA fragmentations in MCF7 and SKOV-3 cells after treatment with the cytotoxic extracts and fractions which were indicative of cell apoptosis. Methyl palmitate and methyl stearate were identified in the hexane leaf extract by GC-MS analysis.

    CONCLUSIONS: The data obtained from the current study demonstrated that the cell death induced by cytotoxic extracts and fractions of A. scabra may be due to apoptosis induction which was characterized by apoptotic morphological changes and DNA fragmentation. The active ingredients in the leaf sub-fraction VLC9 and rhizome fraction RC5 may lead to valuable compounds that have the ability to kill cancer cells but not normal cells.

    Matched MeSH terms: Breast Neoplasms/physiopathology
Filters
Contact Us

Please provide feedback to Administrator (afdal@afpm.org.my)

External Links