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Fulltext Inhibition of Janus Kinase 1 synergizes docetaxel sensitivity in prostate cancer cells

Nalairndran G, Chung I, Abdul Razack AH, Chung FF, Hii LW, Lim WM, et al.

J Cell Mol Med, 2021 Sep;25(17):8187-8200.
PMID: 34322995 DOI: 10.1111/jcmm.16684

Prostate cancer (PCa) is the second most common malignancy and is the fifth leading cause of cancer mortality among men globally. Docetaxel-based therapy remains the first-line treatment for metastatic castration-resistant prostate cancer. However, dose-limiting toxicity including neutropenia, myelosuppression and neurotoxicity is the major reason for docetaxel dose reductions and fewer cycles administered, despite a recent study showing a clear survival benefit with increased total number of docetaxel cycles in PCa patients. Although previous studies have attempted to improve the efficacy and reduce docetaxel toxicity through drug combination, no drug has yet demonstrated improved overall survival in clinical trial, highlighting the challenges of improving the activity of docetaxel monotherapy in PCa. Herein, we identified 15 lethality hits for which inhibition could enhance docetaxel sensitivity in PCa cells via a high-throughput kinome-wide loss-of-function screen. Further drug-gene interactions analyses identified Janus kinase 1 (JAK1) as a viable druggable target with existing experimental inhibitors and FDA-approved drugs. We demonstrated that depletion of endogenous JAK1 enhanced docetaxel-induced apoptosis in PCa cells. Furthermore, inhibition of JAK1/2 by baricitinib and ruxolitinib synergizes docetaxel sensitivity in both androgen receptor (AR)-negative DU145 and PC3 cells, but not in the AR-positive LNCaP cells. In contrast, no synergistic effects were observed in cells treated with JAK2-specific inhibitor, fedratinib, suggesting that the synergistic effects are mainly mediated through JAK1 inhibition. In conclusion, the combination therapy with JAK1 inhibitors and docetaxel could be a useful therapeutic strategy in the treatment of prostate cancers.

Matched MeSH terms: Drug Resistance, Neoplasm/drug effects
Histone deacetylase (HDAC) inhibitors and doxorubicin combinations target both breast cancer stem cells and non-stem breast cancer cells simultaneously

Hii LW, Chung FF, Soo JS, Tan BS, Mai CW, Leong CO

Breast Cancer Res Treat, 2020 Feb;179(3):615-629.
PMID: 31784862 DOI: 10.1007/s10549-019-05504-5

PURPOSE: Breast cancer stem cells (CSCs) are a small subpopulation of cancer cells that have high capability for self-renewal, differentiation, and tumor initiation. CSCs are resistant to chemotherapy and radiotherapy, and are responsible for cancer recurrence and metastasis.
METHODS: By utilizing a panel of breast cancer cells and mammospheres culture as cell-based screening platforms, we performed high-throughput chemical library screens to identify agents that are effective against breast CSCs and non-CSCs. The hit molecules were paired with conventional chemotherapy to evaluate the combinatorial treatment effects on breast CSCs and non-CSCs.
RESULTS: We identified a total of 193 inhibitors that effectively targeting both breast CSCs and non-CSCs. We observed that histone deacetylase inhibitors (HDACi) synergized conventional chemotherapeutic agents (i.e., doxorubicin and cisplatin) in targeting breast CSCs and non-CSCs simultaneously. Further analyses revealed that quisinostat, a potent inhibitor for class I and II HDACs, potentiated doxorubicin-induced cytotoxicity in both breast CSCs and non-CSCs derived from the basal-like (MDA-MB-468 and HCC38), mesenchymal-like (MDA-MB-231), and luminal-like breast cancer (MCF-7). It was also observed that the basal-like breast CSCs and non-CSCs were more sensitive to the co-treatment of quisinostat with doxorubicin compared to that of the luminal-like breast cancer subtype.
CONCLUSION: In conclusion, this study demonstrates the potential of HDACi as therapeutic options, either as monotherapy or in combination with chemotherapeutics against refractory breast cancer.

Matched MeSH terms: Drug Resistance, Neoplasm
Diosgenin, a steroidal saponin, and its analogs: Effective therapies against different chronic diseases

Parama D, Boruah M, Yachna K, Rana V, Banik K, Harsha C, et al.

Life Sci, 2020 Nov 01;260:118182.
PMID: 32781063 DOI: 10.1016/j.lfs.2020.118182

BACKGROUND: Chronic diseases are a major cause of mortality worldwide, and despite the recent development in treatment modalities, synthetic drugs have continued to show toxic side effects and development of chemoresistance, thereby limiting their application. The use of phytochemicals has gained attention as they show minimal side effects. Diosgenin is one such phytochemical which has gained importance for its efficacy against the life-threatening diseases, such as cardiovascular diseases, cancer, nervous system disorders, asthma, arthritis, diabetes, and many more.
AIM: To evaluate the literature available on the potential of diosgenin and its analogs in modulating different molecular targets leading to the prevention and treatment of chronic diseases.
METHOD: A detailed literature search has been carried out on PubMed for gathering information related to the sources, biosynthesis, physicochemical properties, biological activities, pharmacokinetics, bioavailability and toxicity of diosgenin and its analogs.
KEY FINDINGS: The literature search resulted in many in vitro, in vivo and clinical trials that reported the efficacy of diosgenin and its analogs in modulating important molecular targets and signaling pathways such as PI3K/AKT/mTOR, JAK/STAT, NF-κB, MAPK, etc., which play a crucial role in the development of most of the diseases. Reports have also revealed the safety of the compound and the adaptation of nanotechnological approaches for enhancing its bioavailability and pharmacokinetic properties.
SIGNIFICANCE: Thus, the review summarizes the efficacy of diosgenin and its analogs for developing as a potent drug against several chronic diseases.

Matched MeSH terms: Drug Resistance, Neoplasm
JNK signaling in cancer cell survival

Wu Q, Wu W, Fu B, Shi L, Wang X, Kuca K

Med Res Rev, 2019 11;39(6):2082-2104.
PMID: 30912203 DOI: 10.1002/med.21574

c-Jun N-terminal kinase (JNK) is involved in cancer cell apoptosis; however, emerging evidence indicates that this Janus signaling promotes cancer cell survival. JNK acts synergistically with NF-κB, JAK/STAT, and other signaling molecules to exert a survival function. JNK positively regulates autophagy to counteract apoptosis, and its effect on autophagy is related to the development of chemotherapeutic resistance. The prosurvival effect of JNK may involve an immune evasion mechanism mediated by transforming growth factor-β, toll-like receptors, interferon-γ, and autophagy, as well as compensatory JNK-dependent cell proliferation. The present review focuses on recent advances in understanding the prosurvival function of JNK and its role in tumor development and chemoresistance, including a comprehensive analysis of the molecular mechanisms underlying JNK-mediated cancer cell survival. There is a focus on the specific "Yin and Yang" functions of JNK1 and JNK2 in the regulation of cancer cell survival. We highlight recent advances in our knowledge of the roles of JNK in cancer cell survival, which may provide insight into the distinct functions of JNK in cancer and its potential for cancer therapy.

Matched MeSH terms: Drug Resistance, Neoplasm
Fulltext Differential regulation of cell death pathways by the microenvironment correlates with chemoresistance and survival in leukaemia

Qattan MY, Bakker EY, Rajendran R, Chen DW, Saha V, Liu J, et al.

PLoS One, 2017;12(6):e0178606.
PMID: 28582465 DOI: 10.1371/journal.pone.0178606

Glucocorticoids (GCs) and topoisomerase II inhibitors are used to treat acute lymphoblastic leukaemia (ALL) as they induce death in lymphoid cells through the glucocorticoid receptor (GR) and p53 respectively. Mechanisms underlying ALL cell death and the contribution of the bone marrow microenvironment to drug response/resistance remain unclear. The role of the microenvironment and the identification of chemoresistance determinants were studied by transcriptomic analysis in ALL cells treated with Dexamethasone (Dex), and Etoposide (Etop) grown in the presence or absence of bone marrow conditioned media (CM). The necroptotic (RIPK1) and the apoptotic (caspase-8/3) markers were downregulated by CM, whereas the inhibitory effects of chemotherapy on the autophagy marker Beclin-1 (BECN1) were reduced suggesting CM exerts cytoprotective effects. GCs upregulated the RIPK1 ubiquitinating factor BIRC3 (cIAP2), in GC-sensitive (CEM-C7-14) but not in resistant (CEM-C1-15) cells. In addition, CM selectively affected GR phosphorylation in a site and cell-specific manner. GR is recruited to RIPK1, BECN1 and BIRC3 promoters in the sensitive but not in the resistant cells with phosphorylated GR forms being generally less recruited in the presence of hormone. FACS analysis and caspase-8 assays demonstrated that CM promoted a pro-survival trend. High molecular weight proteins reacting with the RIPK1 antibody were modified upon incubation with the BIRC3 inhibitor AT406 in CEM-C7-14 cells suggesting that they represent ubiquitinated forms of RIPK1. Our data suggest that there is a correlation between microenvironment-induced ALL proliferation and altered response to chemotherapy.

Matched MeSH terms: Drug Resistance, Neoplasm/genetics*
Overview of the multifaceted resistances toward EGFR-TKIs and new chemotherapeutic strategies in non-small cell lung cancer

Dzul Keflee R, Leong KH, Ogawa S, Bignon J, Chan MC, Kong KW

Biochem Pharmacol, 2022 Nov;205:115262.
PMID: 36191627 DOI: 10.1016/j.bcp.2022.115262

The role of epidermal growth factor receptor (EGFR) in non-small cell lung cancer (NSCLC) has been vastly studied over the last decade. This has led to the rapid development of many generations of EGFR tyrosine kinase inhibitors (EGFR-TKIs). However, patients treated with third-generation TKIs (osimertinib, avitinib and rociletinib) targeting the EGFR T790M mutation have shown emerging resistances and relapses. Therefore, further molecular understanding of NSCLC mutations, bypass signalling, tumour microenvironment and the existence of cancer stem cells to overcome such resistances is warranted. This will pave the way for designing novel and effective chemotherapies to improve patients' overall survival. In this review, we provide an overview of the multifaceted mechanisms of resistance towards EGFR-TKIs, as well as the challenges and perspectives that should be addressed in strategising chemotherapeutic treatments to overcome the ever-evolving and adaptive nature of NSCLC.

Matched MeSH terms: Drug Resistance, Neoplasm
Reversal of multidrug resistance (MDR) by aspidofractinine-type indole alkaloids

Kam TS, Subramaniam G, Sim KM, Yoganathan K, Koyano T, Toyoshima M, et al.

Bioorg Med Chem Lett, 1998 Oct 06;8(19):2769-72.
PMID: 9873619

A series of indole alkaloids of the aspidofractinine-type was assessed for their potential in reversing MDR in vincristine-resistant KB cells. Of the compounds tested, kopsiflorine, kopsamine, pleiocarpine, 11-methoxykopsilongine, lahadinine A and N-methoxycarbonyl-11,12-methylenedioxy-delta 16,17-kopsinine were found to show appreciable activity.

Matched MeSH terms: Drug Resistance, Neoplasm
Conodiparines A-D, new bisindoles from Tabernaemontana. Reversal of vincristine-resistance with cultured cells

Kam TS, Sim KM, Koyano T, Toyoshima M, Hayashi M, Komiyama K

Bioorg Med Chem Lett, 1998 Jul 07;8(13):1693-6.
PMID: 9873417

Four new bisindoles of the vobasine-iboga type, conodiparines A-D were obtained from Tabernaemontana corymbosa which showed appreciable activity in reversing resistance in vincristine-resistant KB cells.

Matched MeSH terms: Drug Resistance, Neoplasm*
Lack of association between expression of MRP2 and early relapse of colorectal cancer in patients receiving FOLFOX-4 chemotherapy

Mirakhorli M, Shayanfar N, Rahman SA, Rosli R, Abdullah S, Khoshzaban A

Oncol Lett, 2012 Nov;4(5):893-897.
PMID: 23162618

Recurrence following failure of chemotherapy limits the application of high doses of anticancer drugs currently used for eliminating cancerous cells. It has been identified that ATP-binding cassette (ABC) multidrug transporters are associated with chemoresistance, which is a major obstacle in cancer therapy. The present study aimed to investigate the association of pretherapeutic multidrug resistance-associated protein 2 (MRP2) expression with response to chemotherapy in stage II/III colorectal cancer (CRC). Protein expression was determined by immunohistochemical analysis of 50 archival samples from patients who had not received preoperative chemotherapy and radiotherapy. All patients were treated with 5-fluorouracil/leucovorin (FL) plus oxaliplatin (FOLFOX-4) regimen for 6 months following curative resection. During the 12 months of follow-up, local and distant recurrences were observed in 15 (30%) cases, of which 5 occurred at the time of chemotherapy. MRP2 expression was observed in 24 (48%) and 7 (14%) cases in the tumor tissues and matched normal tissues, respectively. A significant difference was observed between the positive expression frequency in the tumor tissues compared to the surrounding normal mucosa (P=0.003). The incidence of recurrence and metastasis for patients in the MRP2-positive group was lower than that in the MRP2-negative group (P>0.05); however, all 5 cases who demonstrated recurrence during their treatment were MRP2-positive (P=0.022). MRP2 expression was not correlated with the clinicopathological markers in this group of patients. Kaplan-Meier analysis revealed that MRP2 expression was not associated with a shorter disease-free survival or overall survival of patients (P>0.05). The results of this study indicated that MRP2 is overexpressed in the course of CRC development and progression. However, expression of MRP2 was not associated with recurrence of patients treated with FL and oxaliplatin in the population studied.

Matched MeSH terms: Drug Resistance, Neoplasm
Fulltext Nutlin-3 sensitizes nasopharyngeal carcinoma cells to cisplatin-induced cytotoxicity

Voon YL, Ahmad M, Wong PF, Husaini R, Ng WT, Leong CO, et al.

Oncol Rep, 2015 Oct;34(4):1692-700.
PMID: 26252575 DOI: 10.3892/or.2015.4177

The small-molecule inhibitor of p53-Mdm2 interaction, Nutlin-3, is known to be effective against cancers expressing wild-type (wt) p53. p53 mutations are rare in nasopharyngeal carcinoma (NPC), hence targeting disruption of p53-Mdm2 interaction to reactivate p53 may offer a promising therapeutic strategy for NPC. In the present study, the effects of Nutlin-3 alone or in combination with cisplatin, a standard chemotherapeutic agent, were tested on C666-1 cells, an Epstein-Barr virus (EBV)-positive NPC cell line bearing wt p53. Treatment with Nutlin-3 activated the p53 pathway and sensitized NPC cells to the cytotoxic effects of cisplatin. The combined treatment also markedly suppressed soft agar colony growth formation and increased apoptosis of NPC cells. The effect of Nutlin-3 on NPC cells was inhibited by knockdown of p53, suggesting that its effect was p53-dependent. Extended treatment with increasing concentrations of Nutlin-3 did not result in emergence of p53 mutations in the C666-1 cells. Collectively, the present study revealed supportive evidence of the effectiveness of combining cisplatin and Nutlin-3 as a potential therapy against NPC.

Matched MeSH terms: Drug Resistance, Neoplasm
Doxorubicin and siRNA Codelivery via Chitosan-Coated pH-Responsive Mixed Micellar Polyplexes for Enhanced Cancer Therapy in Multidrug-Resistant Tumors

Butt AM, Amin MC, Katas H, Abdul Murad NA, Jamal R, Kesharwani P

Mol Pharm, 2016 12 05;13(12):4179-4190.
PMID: 27934479

This study investigated the potential of chitosan-coated mixed micellar nanocarriers (polyplexes) for codelivery of siRNA and doxorubicin (DOX). DOX-loaded mixed micelles (serving as cores) were prepared by thin film hydration method and coated with chitosan (CS, serving as outer shell), and complexed with multidrug resistance (MDR) inhibiting siRNA. Selective targeting was achieved by folic acid conjugation. The polyplexes showed pH-responsive enhanced DOX release in acidic tumor pH, resulting in higher intracellular accumulation, which was further augmented by downregulation of mdr-1 gene after treatment with siRNA-complexed polyplexes. In vitro cytotoxicity assay demonstrated an enhanced cytotoxicity in native 4T1 and multidrug-resistant 4T1-mdr cell lines, compared to free DOX. Furthermore, in vivo, polyplexes codelivery resulted in highest DOX accumulation and significantly reduced the tumor volume in mice with 4T1 and 4T1-mdr tumors as compared to the free DOX groups, leading to improved survival times in mice. In conclusion, codelivery of siRNA and DOX via polyplexes has excellent potential as targeted drug nanocarriers for treatment of MDR cancers.

Matched MeSH terms: Drug Resistance, Neoplasm
Exome sequencing and array-based comparative genomic hybridisation analysis of preferential 6-methylmercaptopurine producers

Chua EW, Cree S, Barclay ML, Doudney K, Lehnert K, Aitchison A, et al.

Pharmacogenomics J, 2015 Oct;15(5):414-21.
PMID: 25752523 DOI: 10.1038/tpj.2015.9

Preferential conversion of azathioprine or 6-mercaptopurine into methylated metabolites is a major cause of thiopurine resistance. To seek potentially Mendelian causes of thiopurine hypermethylation, we recruited 12 individuals who exhibited extreme therapeutic resistance while taking azathioprine or 6-mercaptopurine and performed whole-exome sequencing (WES) and copy-number variant analysis by array-based comparative genomic hybridisation (aCGH). Exome-wide variant filtering highlighted four genes potentially associated with thiopurine metabolism (ENOSF1 and NFS1), transport (SLC17A4) or therapeutic action (RCC2). However, variants of each gene were found only in two or three patients, and it is unclear whether these genes could influence thiopurine hypermethylation. Analysis by aCGH did not identify any unusual or pathogenic copy-number variants. This suggests that if causative mutations for the hypermethylation phenotype exist they may be heterogeneous, occurring in several different genes, or they may lie within regulatory regions not captured by WES. Alternatively, hypermethylation may arise from the involvement of multiple genes with small effects. To test this hypothesis would require recruitment of large patient samples and application of genome-wide association studies.

Matched MeSH terms: Drug Resistance, Neoplasm
Aspidofractinine and Eburnane Alkaloids from a North Borneo Kopsia. Ring-Contracted, Additional Ring-Fused, and Paucidactine-Type Aspidofractinine Alkaloids from K. pauciflora

Yap WS, Gan CY, Sim KS, Lim SH, Low YY, Kam TS

J Nat Prod, 2016 Jan 22;79(1):230-9.
PMID: 26717050 DOI: 10.1021/acs.jnatprod.5b00992

Eleven new indole alkaloids (1-11) comprising seven aspidofractinine and four eburnane alkaloids, were isolated from the stem-bark extract of Kopsia pauciflora occurring in Malaysian Borneo. The aspidofractinine alkaloids include a ring-contracted, an additional ring-fused, a paucidactine regioisomer, two paucidactine, and one kopsine alkaloid. The structures of several of these alkaloids were also confirmed by X-ray diffraction analyses. The bisindole alkaloids isolated, norpleiomutine and kopsoffinol, showed in vitro growth inhibitory activity against human PC-3, HCT-116, MCF-7, and A549 cells and moderate effects in reversing multidrug-resistance in vincristine-resistant human KB cells.

Matched MeSH terms: Drug Resistance, Neoplasm/drug effects
Corynanthean, eburnan, secoleuconoxine, and pauciflorine alkaloids from Kopsia pauciflora

Gan CY, Yoganathan K, Sim KS, Low YY, Lim SH, Kam TS

Phytochemistry, 2014 Dec;108:234-42.
PMID: 25442910 DOI: 10.1016/j.phytochem.2014.09.014

Eleven indole alkaloids, comprising four corynanthean, two eburnane, one aspidofractinine, one secoleuconoxine, one andranginine, and two pauciflorine type alkaloids were isolated from the stem-bark and leaf extracts of Kopsia pauciflora. Their structures were determined using NMR and MS analyses. The catharinensine type alkaloid kopsirensine B and the secoleuconoxine alkaloid arboloscine A showed moderate to weak activity in reversing MDR in vincristine-resistant KB cells. The alkaloid content was markedly different compared to that of a sample from Malaysian Borneo.

Matched MeSH terms: Drug Resistance, Neoplasm/drug effects
Macroline, akuammiline, sarpagine, and ajmaline alkaloids from Alstonia macrophylla

Lim SH, Low YY, Sinniah SK, Yong KT, Sim KS, Kam TS

Phytochemistry, 2014 Feb;98:204-15.
PMID: 24342109 DOI: 10.1016/j.phytochem.2013.11.014

A total of seventeen alkaloids, comprising six macroline (including alstofolinine A, a macroline indole incorporating a butyrolactone ring-E), two ajmaline, one sarpagine, and eight akuammiline alkaloids, were isolated from the stem-bark and leaf extracts of the Malayan Alstonia macrophylla. The structure and relative configurations of these alkaloids were established using NMR, MS and in several instances, confirmed by X-ray diffraction analysis. Six of these alkaloids were effective in reversing multidrug-resistance (MDR) in vincristine-resistant KB cells.

Matched MeSH terms: Drug Resistance, Neoplasm/drug effects*
Rhazinilam-Leuconolam-Leuconoxine Alkaloids from Leuconotis griffithii

Gan CY, Low YY, Thomas NF, Kam TS

J Nat Prod, 2013 May 24;76(5):957-64.
PMID: 23647487 DOI: 10.1021/np400214y

Eight new indole alkaloids (1-8) belonging to the rhazinilam-leuconolam-leuconoxine group, in addition to 52 other alkaloids, were isolated from the stem-bark extract of Leuconotis griffithii, viz., nor-rhazinicine (1), 5,21-dihydrorhazinilam-N-oxide (2), 3,14-dehydroleuconolam (3), and leuconodines A-E (4-8). The structures of these alkaloids were determined using NMR and MS analyses and in some instances confirmed by X-ray diffraction analyses. Alkaloids 1, 5, and 7 showed only moderate to weak cytotoxicity toward KB cells (IC50 12-18 μg/mL), while 8 showed moderate activity in reversing MDR in vincristine-resistant KB cells.

Matched MeSH terms: Drug Resistance, Neoplasm/drug effects
Strychnan and secoangustilobine A type alkaloids from Alstonia spatulata. Revision of the C-20 configuration of scholaricine

Tan SJ, Low YY, Choo YM, Abdullah Z, Etoh T, Hayashi M, et al.

J Nat Prod, 2010 Nov 29;73(11):1891-7.
PMID: 21043460 DOI: 10.1021/np100552b

A total of 25 alkaloids were isolated from the leaf and stem-bark extracts of Alstonia spatulata, of which five are new alkaloids of the strychnan type (alstolucines A-E, 1-5) and the other, a new alkaloid of the secoangustilobine A type (alstolobine A, 6). The structures of these alkaloids were established using NMR and MS analysis and, in the case of alstolucine B (2), also confirmed by X-ray diffraction analysis. A reinvestigation of the stereochemical assignment of scholaricine (13) by NMR and X-ray analyses indicated that the configuration at C-20 required revision. Alkaloids 1, 2, 6, 7, 9, 10, and 13 reversed multidrug resistance in vincristine-resistant KB cells.

Matched MeSH terms: Drug Resistance, Neoplasm/drug effects
Leucoridines A-D, cytotoxic Strychnos-Strychnos bisindole alkaloids from Leuconotis

Gan CY, Etoh T, Hayashi M, Komiyama K, Kam TS

J Nat Prod, 2010 Jun 25;73(6):1107-11.
PMID: 20515042 DOI: 10.1021/np1001187

Four new bisindole alkaloids of the Strychnos-Strychnos type, leucoridines A-D (1-4), were isolated from the stem-bark extract of Leuconotis griffithii. Alkaloids 1-4 showed moderate cytotoxicity against drug-sensitive and vincristine-resistant human KB cells.

Matched MeSH terms: Drug Resistance, Neoplasm
Leucophyllidine, a cytotoxic bisindole alkaloid constituted from the union of an eburnan and a new vinylquinoline alkaloid

Gan CY, Robinson WT, Etoh T, Hayashi M, Komiyama K, Kam TS

Org. Lett., 2009 Sep 3;11(17):3962-5.
PMID: 19708704 DOI: 10.1021/ol9016172

A cytotoxic bisindole alkaloid possessing an unprecedented structure constituted from the union of an eburnan half and a novel vinylquinoline alkaloid has been isolated from Leuconotis griffithii. The structure was established by analysis of the spectroscopic data and confirmed by X-ray diffraction analysis. A possible biogenetic pathway to the novel quinolinic coupling partner is presented from an Aspidosperma precursor.

Matched MeSH terms: Drug Resistance, Neoplasm/drug effects
A cycloartane incorporating a fused tetrahydrofuran ring and a cytotoxic lactam from Monocarpia marginalis

Lim SH, Mahmood K, Komiyama K, Kam TS

J Nat Prod, 2008 Jun;71(6):1104-6.
PMID: 18462006 DOI: 10.1021/np800123g

A new cycloartane, monocarpinine (1), incorporating a fused tetrahydrofuranyl ring, and a cytotoxic tetracyclic lactam, monomarginine (2), were isolated from a stem bark extract of the Malayan species Monocarpia marginalis. The structures of these compounds were determined using NMR and MS analysis. Monomarginine (2) showed appreciable cytotoxicity toward human KB (both drug-sensitive and drug-resistant) and Jurkat cells.

Matched MeSH terms: Drug Resistance, Neoplasm/drug effects

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