Radiation Biology

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SU_37_2370 - RAD51 is a potential marker for prognosis and regulates proliferation in pancreatic cancer

Sunday, October 21
1:15 PM - 2:45 PM
Location: Innovation Hub, Exhibit Hall 3

RAD51 is a potential marker for prognosis and regulates proliferation in pancreatic cancer
Z. G. Ren; Fudan university cancer hospital, Shanghai, China

Purpose/Objective(s): DNA damage and repair pathway has been considered a promising target for developing strategies against cancer. Rad51, also known as RecA ,is a recombinase that executes the critical step in homologous recombination. Rad51 has lately received much attention due to its implication in tumor progression, and its decisive role in tumor resistance to chemotherapy. However, its role in pancreatic cancer has seldom been discussed. In this present study, we examined the correlation of Rad51 with Kras mutation, the contribution of Rad51 to proliferation and glucose metabolism reprogramming in pancreatic cancer.

Materials/Methods: TCGA dataset analysis was used to explore the clinical correlation of Rad51 expression with overall survival in pancreatic cancer. The human pancreatic cancer cell lines PANC-1 and MiaPaCa-2 were obtained from ATCC and are cultured according to standard protocols that provided by ATCC. Lentivirus mediated transfection method was used to silence Rad51 expression. Quantitative real-time PCR and western blot analysis validated the efficacy of knockdown effect. CCK8 proliferation assay was performed to confirm the influence of Rad51 on cell viability. The relationship of Rad51 with Kras, ROS, HIFIa, glycolytic genes (Glut1, HK2 and LDHA) was assessed by using quantitative real-time PCR and western blot analysis. The correlation of Rad51 was aerobic glycolysis was investigated by Seahorse ECAR measurement.

Results: Rad51 expression predicted prognosis in pancreatic cancer and regulated proliferation of pancreatic cancer cells. Rad51 was a downstream target of oncogenic Kras and regulated ROS production and HIFIa protein levels. Rad51 regulated aerobic glycolysis in pancreatic caner cells and positively correlated with glycolytic genes in pancreatic cancer patients.

Conclusion: Rad51, a downstream target of oncogenic Kras mutation, promotes pancreatic cancer cell proliferation. Furthermore, Rad51 regulated aerobic glycolysis by targeting Hypoxia inducible factor 1a (HIFIa). Taken together, out present study uncovered novel functions of DNA repair machinery in cancer cell metabolism reprogramming and provided novel targets for pancreatic cancer treatment.

Author Disclosure: z. Ren: None.

zhi-gang Ren

Biography:
NAME: Zhigang Ren, M.D.
WORKING ADDRESS
Department of Radiation Oncology
Fudan University Cancer Hospital
270 Dong An Road
Shanghai, 200032, P.R.China
PHONE
Mobile phone:+8613636473249
E-MAIL
Zhigang-ren@163.com
PERSONAL INFORMATION
Gender: Male
Date of Birth: Feb. 09, 1973,
Place of Birth: Hebei Province, P.R.China
Marital Status: Married
PROFESSIONAL EXPERIENCE
January.2016- Work as an Associate chief physician in Fudan University, Cancer hospital, Shanghai.
July.2009-December 2015 Work as an attending in Fudan University, Cancer hospital, Shanghai.
Augst.2004-Augst.2006 Employed as an attending in department of radiation Oncology Dongfeng County General Hospital, Hubei province.
Augst.1996-Sept.2001 Work as an resident and attending in Dongfeng County General Hospital, Hubei province.
PROFESSIONAL SKILLS
Clinical Expertise:
Combination of chemo- and radiotherapies on pancreatic cancer, lung cancer, esophageal cancer, head & neck cancers, gastrointestinal tract cancers, Liver tumors, breast cancer, urinary tract cancer, and so on.
Research Skills:
Research training in Clinical Trials and Basic Medicine.
Computer Skills:
Familiar with Window system, Microsoft Office package, Photoshop, statistical software such as SPSS, etc. experienced in the use of the Internet for science information.
AREAS OF INTEREST
 Intensity-modulated radiation therapy (IMRT); Biologically conformal radiation therapy (BCRT).
 Clinical trial of radiation oncology.
 Computer optimization of clinical decision-making (EUD, TCP and NTCP) and normal tissue injure.

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