Skills (26)
Research experience
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Aug 2012–
presentResearch: Postdoctoral Reseaech Fellow
Chinese Academy of Sciences, Changchun China · CIACChina · Changchun -
Jan 2012
Research: Northeast Normal University
Northeast Normal University · Membrane Channel Research LaboratoryChina · Changchun -
Jan 2011
Research: Jilin University
Jilin UniversityChina · Jilin -
Aug 2008–
Jul 2012Research: Natural product Chemistry/Cancer Biology, Cell signaling pathways
Northeast Normal University · Tonghui Ma LabChina · Changchun
Education
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Aug 2012
Chinese Academy of Sciencs, Changchun, China
Cell signaling pathwaysl; Cancer Nanotechnology; Drug Delivery · Postdoctoral Research FellowChina · Changchun -
Aug 2008–
Jul 2012Northeast Normal University Changchun, China
PhDChina · Changchun -
Aug 2005–
Jul 2008Bahauddin Zakariya University, Multan, Pakistan
M.PhilPakistan · Multan
Awards & achievements
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Aug 2012Scholarship: Awardee of Postdoctoral Research Fellow at CIAC Chinese Academy of Sciences
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Jul 2012Award: awardee of an incentive award on research publications during PhD studies by Central Research Laboratory of Bethune Second Hospital, Jilin University Changchun, China amounting 20, 000 RMB (30,0000 PKR).
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Apr 2012Award: Awardee of Scholarship and Travel grant (sponsored by F. Hoffman La Roche) WIN Symposium 2012, Paris France.
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Aug 2008Scholarship: Cultural Exchange Scholarship (MOE, Pakistan) for Doctoral degree
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Aug 2007Scholarship: Awardee of merit scholarship by Bahauddin Zakariya University for M. Phil. studie
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Jun 2006Scholarship: Awardee of an Indigenous PhD scholarship (Phase IV, 2006) from Higher Education Commission of Pakistan (No availed).
Other
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LanguagesEnglish
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Scientific Memberships1. European Society for Medical Oncology (ESMO) Switzerland
2. Asian Pacific Organization of Cancer Prevention (APOCP) Korea
3. National Academy of Young Scientist (NAYS) Pakistan
4. Asia-Pacific Chemical, Biological& Environmental Engineering Society (APCBEES) Member NO.: 100624. Thailand.
5. Society for Medicinal Plant and Natural Product Research (G.A.) Gesellschaft für Arzneipflanzen- und Naturstoff-Forschung e.V, Muenster, Germany -
Journal RefereesT?p chí Qu?n Lý Kinh t?
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Other InterestsCancer Research, Oncogene, Cell death and differentiation, N/A
Publications (34) View all
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Article: Antiproliferative and apoptotic effects of pinocembrin in human prostate cancer cells
Bangladesh Journal of Pharmacology 05/2013; · 0.63 Impact Factor -
Article: Eriocalyxin B inhibits proliferation and induces apoptosis through downregulation of Bcl-2 and activation of caspase-3 in human bladder cancer cells
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ABSTRACT: Eriocalyxin B (EriB) has been shown to possess promising anticancer potential against various cancer cells. However, its effect against bladder cancer cells remained unexplored. In this study, for the first time, we investigated the effects of EriB on cell proliferation, cell cycle, and apoptosis in bladder cancer T24 cells. In order to examine the effects of EriB on cell proliferation, cell cycle, and apoptosis, we performed MTT assay, flow cytometric analysis and western blot. The results revealed that EriB decreased the cell viability of T24 cells. Flow cytometric analysis demonstrated that EriB markedly induced apoptosis of T24 cells and arrested cell cycle at G2/M phase in a dose-dependent manner. Further characterization showed that EriB involved in the down-regulation of Bcl-2 and activation of caspase-3 before culminating in apoptosis in EriB-treated T24 cells. These in vitro results suggested that EriB should be further examined for in vivo activity in human bladder cancer.Bangladesh Journal of Pharmacology 03/2013; 8(2):116-123. · 0.63 Impact Factor -
Chapter: Natural Compounds and Their Role in Autophagic Cell Signaling Pathways
02/2013; , ISBN: 980-953-307-971-9 -
Article: Lentivirus-mediated shRNA targeting decoy receptor 3 (DcR3) inhibits proliferation and augments apoptosis in pancreatic cancer Capan-1 cells
[show abstract] [hide abstract]
ABSTRACT: Pancreatic cancer is one of the most dismal malignancies with the actual 5-year survival of only 10 to 20%. Decoy receptor 3 (DcR3) is highly expressed in various cancer cells and plays a significant role in immune suppression and tumor progression. However, how DcR3 expression is modulated in pancreatic cancer cells is enigmatic. The aim of this study was to characterize the expression of DcR3 in pancreatic carcinoma and to evaluate the role of DcR3 in cell proliferation and apoptosis, which may lead to the development of novel treatments for this disease. In the present study, we examined five cell lines including three cell lines from pancreatic cancer (SW1990, Capcan-1 and PANC-1) and two cell lines from colon cancer (HCT116 and RKO) for DcR3 expression by reverse transcriptase-polymerase chain reaction (RT-PCR) and quantitative real time PCR. 3′-(4, 5 dimethyl-thiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay and flow cytometric analysis were used to measure cell proliferation and apoptosis, respectively in the human pancreatic cancer Capan-1 cells. The human pancreatic cancer Capan-1 cell line was first infected with lentivirus-mediated shRNA and then analyzed by real-time PCR, and the results were further confirmed by Western blotting. DcR3 protein in our experimental results showed significant expression among the pancreatic cancer cell lines and their decreased expression by lentivirus-mediated shRNA resulted in the inhibition of cell proliferation and augmentation of apoptosis. In conclusion, these findings suggest that lentivirus-mediated gene therapy targeting DcR3 is a potential and attractive strategy for the treatment of pancreatic cancer.African journal of pharmacy and pharmacology 02/2013; 7(5):203-210. · 0.84 Impact Factor -
Article: Alantolactone Induces Apoptosis in HepG2 Cells through GSH Depletion, Inhibition of STAT3 Activation, and Mitochondrial Dysfunction.
[show abstract] [hide abstract]
ABSTRACT: Signal transducer and activator of transcription 3 (STAT3) constitutively expresses in human liver cancer cells and has been implicated in apoptosis resistance and tumorigenesis. Alantolactone, a sesquiterpene lactone, has been shown to possess anticancer activities in various cancer cell lines. In our previous report, we showed that alantolactone induced apoptosis in U87 glioblastoma cells via GSH depletion and ROS generation. However, the molecular mechanism of GSH depletion remained unexplored. The present study was conducted to envisage the molecular mechanism of alantolactone-induced apoptosis in HepG2 cells by focusing on the molecular mechanism of GSH depletion and its effect on STAT3 activation. We found that alantolactone induced apoptosis in HepG2 cells in a dose-dependent manner. This alantolactone-induced apoptosis was found to be associated with GSH depletion, inhibition of STAT3 activation, ROS generation, mitochondrial transmembrane potential dissipation, and increased Bax/Bcl-2 ratio and caspase-3 activation. This alantolactone-induced apoptosis and GSH depletion were effectively inhibited or abrogated by a thiol antioxidant, N-acetyl-L-cysteine (NAC). The data demonstrate clearly that intracellular GSH plays a central role in alantolactone-induced apoptosis in HepG2 cells. Thus, alantolactone may become a lead chemotherapeutic candidate for the treatment of liver cancer.BioMed research international. 01/2013; 2013:719858.
