MiR-122 Induces Radiosensitization in Non-Small Cell Lung Cancer Cell Line

نویسندگان

  • Debin Ma
  • Hui Jia
  • Mengmeng Qin
  • Wenjie Dai
  • Tao Wang
  • Erguang Liang
  • Guofu Dong
  • Zuojun Wang
  • Zhiyuan Zhang
  • Fan Feng
  • Y-h. Taguchi
چکیده

MiR-122 is a novel tumor suppresser and its expression induces cell cycle arrest, or apoptosis, and inhibits cell proliferation in multiple cancer cells, including non-small cell lung cancer (NSCLC) cells. Radioresistance of cancer cell leads to the major drawback of radiotherapy for NSCLC and the induction of radiosensitization could be a useful strategy to fix this problem. The present work investigates the function of miR-122 in inducing radiosensitization in A549 cell, a type of NSCLC cells. MiR-122 induces the radiosensitization of A549 cells. MiR-122 also boosts the inhibitory activity of ionizing radiation (IR) on cancer cell anchor-independent growth and invasion. Moreover, miR-122 reduced the expression of its targeted genes related to tumor-survival or cellular stress response. These results indicate that miR-122 would be a novel strategy for NSCLC radiation-therapy.

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-96 induced non-small-cell lung cancer progression through competing endogenous RNA network and affecting EGFR signaling pathway

Objective(s): Non-small cell lung cancer (NSCLC) has become a serious global health problem in the 21st century, and tumor proliferation and metastasis are the leading causes of death in patients  with lung cancer. The present study aimed to verify the function of miR-96 and miR-96 in relation to competing with endogenous RNA regulatory network in NSCLC progression inc...

متن کامل

Dihydroartemisinin increases radiosensitivity of A549 lung cancer cells

Background: Radiotherapy is the gold standard in the treatment of lung cancer. However, the radiosensitization of cancerous cells requires further improvement. Here, we investigated the effect of dihydroartemisinin (DHA) on the radiosensitization of non-small cell lung cancer (NSCLC) cells. Methods: Cell proliferation and cell cycle assays were carried out using A549 cells exposed to DHA. The e...

متن کامل

Inhibition of miR-22 enhanced the efficacy of icotinib plus pemetrexed in a rat model of non-small cell lung cancer

Objective(s): To investigate the role of miR-22 in the efficacy of combined icotinib (BPI-2009H) and pemetrexed (LY-231514) on tumor growth and apoptosis in rats with non-small cell lung cancer (NSCLC).Materials and Methods: Rats were injected with HCC827 cells, which were transfected with anti-miR-22, followed by the treatment of BPI-20...

متن کامل

Study of Antimetastatic Effect of Genistein Through Inhibition of Expression of Matrix Metalloproteinase in A-549 Cell Line

The lung cancer is one of the most dangerous cancers and is also the leading cause of cancer death worldwide, accounting for about 1.3 million deaths annually. However in clinical practice, lung cancer therapies commonly do with chemotherapy, although it is hard because the lung cancer may progress to metastasis stage. The metastasis of lung cancer is highly dependent of expression of matrix me...

متن کامل

miR-122 inhibits metastasis and epithelial–mesenchymal transition of non-small-cell lung cancer cells

miR-122 may function as a novel tumor suppressor. Expression of miR-122 could suppress the proliferation of multi-kinds of human cancer cell lines. In this work, expression of miR-122 via adenoviral vector in non-small-cell lung cancer (NSCLC) cells reduces the number of invasion and migration cells. miR-122 attenuates the epithelial-mesenchymal transition process, which mediates cancer cells m...

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 16  شماره 

صفحات  -

تاریخ انتشار 2015