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  1. Fulltext ZFP36L2 silencing increases sensitivity to Temolozomide via G2M cell cycle arrest and BAX mediated apoptosis
    Che Mat M. F., Mohamad Hanif E. A., Abdul Murad N. A., Ibrahim K., Harun R.
    Malaysian Journal of Medicine and Health Sciences, 2019;15(102):11-11.
    MyJurnal
    Introduction: The mortality rate of glioma patients particularly with glioblastoma multiforme (GBM) remains high even with advancements in the multimodality treatment. This is partly due to chemoresistance of the glioma cells towards drug treatment which finally reduced the survival of GBM patients. In this study, we determined the chemosensitisation and oncogenic characteristics of ZFP36L2 in LN18 GBM cells using RNA interference (RNAi). Methods: Meta-analysis of microarray datasets was used to identify the druggable genes responsive to GBM chemosensitivity. Subsequently, the genes were validated using RNAi screening [pooled small interference RNA (siRNA)]. Temozolomide- resistant LN18 cells were used to evaluate the effects of gene silencing on chemosensitisation to the sub-lethal dose (1/10 of IC50) of temozolomide. Assays such as cell viability, proliferation, migration and invasion and apoptosis assays were carried out. The apoptosis pathway underlying chemosensitisation by ZFP36L2 siRNA was determined using a human apoptosis array kit. Statistical analyses were performed using one-way analysis of variance. Results: ZFP36L2 was identified as a potential marker of GBM based on the meta-analysis and RNAi screening. ZFP36L2 knockdown lead to 1) Apoptosis induction (p < 0.05) 2) Reduced cell migration (p < 0.05) 3) Reduced up to 82% of cell invasion (p < 0.01) and 4) Decreased cellular proliferation in siZFP36L2-treated LN18 cells. Downstream analysis showed that the sub-lethal dose of temozolomide caused major upregulation of BCL2-associated X, apoptosis regulator (BAX). Conclusion: ZFP36L2 is oncogenic and chemosensitive thus may contribute to gliomagenesis through cell proliferation, migration, invasion and apoptosis. RNAi therapy in combination with chemotherapy treatment such as temozolomide may serve as potential therapeutic approach in the future.
  2. High sensitivity C-reactive protein (hsCRP): Its relationship with metabolic syndrome and Framingham Risk Score
    Zahari Sham SY, Hanif E, Thambiah SC, Samsudin IN, Mohd Noor S, Osman M, et al.
    Malays J Pathol, 2021 04;43(1):33-40.
    PMID: 33903303
    INTRODUCTION: Cardiovascular disease (CVD) remains the leading cause of death in Malaysia. Identification of asymptomatic at-risk individuals is often achieved by means of a risk prediction algorithm. Traditional CVD risk factors and their associated algorithms are, however, limited by residual CVD risk. High sensitivity C-reactive protein (hsCRP) has emerged as a novel CVD risk factor. This study aimed to evaluate hsCRP as an adjunct CVD risk marker among the adult Malaysian population by determining its correlation with the Framingham Risk Score (FRS). Comparison analyses were done according to sociodemographic, clinical and laboratory factors and between subjects with and without Metabolic Syndrome (MetS).

    METHOD: This cross-sectional study involved eighty-three (n=83) adults attending a health screening program at Universiti Putra Malaysia (UPM). Demographic data, anthropometric measurements and blood samples for fasting blood glucose (FBG), fasting lipid profile (FSL), glycated haemoglobin (HbA1c) and hsCRP were taken. Respondents were grouped according to FRS and the Joint Interim Statement into 10-year CVD risk categories (low, intermediate and high) and MetS, respectively.

    RESULTS: hsCRP was significantly increased in patients with high body mass index (BMI) (p=0.001), at-risk waist circumference (WC) (p=0.001) and MetS (p=0.009). Spearman's correlation coefficient showed a significant positive correlation between hsCRP level and total FRS score (r=0.26, p<0.05) and HDL-C score (r=0.22, p<0.05).

    CONCLUSION: The significant difference of hsCRP levels across obesity levels and MetS with its modest correlation with FRS scores supported the adjunctive role of hsCRP in CVD risk prediction, most likely capturing the inflammatory pathological aspect and thus partly accounting for the residual CVD risk.

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