mir-129-5p Attenuates Irradiation-Induced Autophagy and Decreases Radioresistance of Breast Cancer Cells by Targeting HMGB1

نویسندگان

  • Jing Luo
  • Jie Chen
  • Li He
چکیده

BACKGROUND This study aimed to determine the role of miR-129-5p in irradiation-induced autophagy in breast cancer cells and to investigate its downstream regulation in autophagy-related radiosensitivity. MATERIAL AND METHODS Relative miR-129-5p expression in breast cancer cell lines MCF-7, MDA-MB-231, BT474, and BT549, and in 1 non-tumorigenic breast epithelial cell line, MCF-10A, was compared. The effect of miR-129-5p on irradiation-induced autophagy and radiosensitivity of the cancer cells was explored. The regulative effect of miR-129-5p on HMGB1 and the functional role of this axis in autophagy and radiosensitivity were also studied. RESULTS Ectopic expression of miR-129-5p sensitized MDA-MD-231 cells to irradiation, while knockdown of miR-129-5p reduced radiosensitivity of MCF-7 cells. MiR-129-5p overexpression inhibited irradiation-induced autophagy. HMGB1 is a direct functional target of miR-129-5p in breast cancer cells. MiR-129-5p may suppress autophagy and decrease radioresistance of breast cancer cells by targeting HMGB1. CONCLUSIONS The miR-129-5p/HMGB1 axis can regulate irradiation-induced autophagy in breast cancer and might be an important pathway in regulating radiosensitivity of breast cancer cells.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

MiR-200c inhibits autophagy and enhances radiosensitivity in breast cancer cells by targeting UBQLN1.

Radioresistance is a major challenge during the treatment of breast cancer. A further understanding of the mechanisms of radioresistance could provide strategies to address this challenge. In our study, we compared the expression of miR-200c in four distinct breast cancer cell lines: two representative basal cancer cells (MDA-MB-231 and BT549) vs. two representative luminal cancer cells (MCF-7 ...

متن کامل

MiR-490-5p Functions as an OncomiR in Breast Cancer by Targeting NFATc4

Breast cancer is a serious health problem worldwide in women. MicroRNAs are small non-coding RNAs of 18–25 nucleotides in length that post-transcriptionally modulate gene expression. MiR-490 has been reported as a tumor suppressor and oncomiR microRNA in breast cancer with two separate targets, NFAT and Rho. NFAT is one of the targets for miR-490 but the relationship between hsa</e...

متن کامل

Correlation between Expression of hsa-miR-490-5p and NFAT5 in Peripheral Blood Mononuclear Cell Obtained from Breast Cancer Patients

Breast cancer is a complex genetic disease that has an average annual incidence of two million people and the second leading cause of death among women all over the world. Micro-RNAs are consistently reported to regulate gene expression in all cancers. The present study, the correlation between the expression of hsa-miR-490-5p and nuclear factor of activated T-cells 5 (NFAT5) in breast cancer w...

متن کامل

MicroRNA-410-3p attenuates gemcitabine resistance in pancreatic ductal adenocarcinoma by inhibiting HMGB1-mediated autophagy

Gemcitabine-based chemotherapy is the most common treatment option for pancreatic ductal adenocarcinoma (PDAC). However, it offers little therapeutic value in many cases due to the rapid development of chemoresistance. MicroRNAs (miRNAs) have been found to play pivotal roles in the chemotherapeutic resistance of PDAC. We found that miR-410-3p was significantly down-regulated in human pancreatic...

متن کامل

The downregulation of ATG4B mediated by microRNA-34a/34c-5p suppresses rapamycin-induced autophagy

Objective(s): Autophagy-related 4B (ATG4B) plays an important role in the process of autophagy induction. However, the molecular events that govern the expression of ATG4B in this process are not well known. Materials and Methods: Human ATG4B 3'-UTR region (1377 nt) containing miR-34a/miR-34c-5p binding site was amplified by PCR. Luciferase assay was used to assess the activity of reporter gene...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره 21  شماره 

صفحات  -

تاریخ انتشار 2015