Regulation of miR-181 on chemotherapy-resistant cervical cancer cells

نویسندگان

  • Wenlian Liu
  • Ping Li
  • Qian Xu
  • Changxiu Wang
چکیده

MiR-181 was highly expressed in lung cancer cells of cisplatin-resistance. In this study, we sought to explore the connection of miR-181 expression with cell proliferation, invasion and apoptosis in cervical cancer cells. Real-time polymerase chain reaction and Western blot were performed to determine the expression level of miR181 at mRNA and protein level. Then MTT and flow cytometry were respectively used to explore the proliferation, apoptosis in cervical cancer cells, lactic dehydrogenase assay was performed to test the cytotoxicity. The results suggested that overexpression of miR-181 significantly increased the proliferation and decreased apoptosis of cytotoxicity cervical cancer cells compared with the control group. Moreover, LDH activity of miR-181-overexpressed cells was significantly decreased, suggesting reduction of the cytotoxicity and the increase of drugs-resistance. These results proved that miR-181 could be tightly involved in protection of cervical cancer. This study revealed the key roles of miR-181 and its potential in treating cervical cancer.

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-181 regulates cisplatin-resistant non-small cell lung cancer via downregulation of autophagy through the PTEN/PI3K/AKT pathway

A number of miRNAs have been found to be abnormally expressed or mutated in numerous cancers and thus, are considered to act as oncogenes or tumor suppressor genes. The aim of the present study was to investigate the effect of miR-181 on cisplatin-resistant non-small cell lung cancer (NSCLC). In patients with cisplatin-resistant NSCLC, miR-181 expression was found to be markedly decreased. In a...

متن کامل

miR‐25‐3p reverses epithelial‐mesenchymal transition via targeting Sema4C in cisplatin‐resistance cervical cancer cells

Acquisition of epithelial-mesenchymal transition (EMT) has recently been proposed as an important contributor of drug resistance in cervical cancer cells. However, the underlying mechanisms are still unclear. MicroRNAs play a crucial role in regulating EMT. The aim of this study was to explore the potential role of miR-25-3p in regulating EMT in cisplatin-resistant (CR) cervical cancer cells. T...

متن کامل

Up-regulation of microRNA-664 inhibits cell growth and increases cisplatin sensitivity in cervical cancer.

BACKGROUND Cervical cancer is one of the leading causes of cancer-related death in woman worldwide. In the present study, we investigated the role of microRNA 664 (miR-664) in regulating cancer migration and chemotherapy sensitivity in cervical cancer. METHODS Quantitative real-time PCR (qPCR) was used to assess the mRNA levels of miR-664 in both cervical cancer cell lines and cancer tissues ...

متن کامل

MicroRNA-181 targets Yin Yang 1 expression and inhibits cervical cancer progression.

Dysregulated expression of microRNAs (miRNAs) has been observed in numerous types of human cancer, including cervical cancer (CC). The present study aimed to elucidate the expression and roles of miR‑181 in cervical cancer tissues and cells. HeLa cells with a stable overexpression of miR‑181 were generated and injected subcutaneously into the front legs of nude mice. Functional assays revealed ...

متن کامل

مطالعه ارتباط مقاومت به تراستوزوماب با بیان نسبی میکرو‌آر‌ان‌ای ۱۴۱ (miR-141 ) در سلول‌های انسانی سرطانی پستان BT-474

Background and Aim: Resistance to trastuzumab has been a critical barrier to targeted therapy of HER 2-positive (Human Epidermal Growth Factor Receptor 2) breast cancers. MicroRNAs (miRNAs) are known as decisive core regulators of drug resistance that modulate the epithelial-to-mesenchymal transition (EMT) and cancer-related immune responses. The present study aimed at examining the expression ...

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   شماره 

صفحات  -

تاریخ انتشار 2016