MicroRNA-326 suppresses the proliferation, migration and invasion of cervical cancer cells by targeting ELK1

نویسندگان

  • Ping Zhang
  • Feng Kong
  • Xinchao Deng
  • Yunhai Yu
  • Congzhe Hou
  • Tingting Liang
  • Lin Zhu
چکیده

Although microRNAs (miRNAs or miRs) are able to function as oncogenes or tumor suppressors, the role of miR-326 in regulating human cervical cancer cells remains unclear. In the present study, the expression of miR-326 was identified to be downregulated in cervical cancer cell lines and primary tumor samples, and the overexpression of miR-326 decreased cell proliferation, migration and invasion in cervical cell lines. Bioinformatics prediction and experimental validation results revealed that the function of miR-326 was achieved by targeting and repressing ETS domain-containing protein Elk-1 (ELK1) expression. ELK1 was targeted directly by miR-326, which was downregulated in human cervical cancer tissues compared with that in adjacent normal tissues. The results of the present study suggest that miR-326, a potential tumor suppressor, may be used in the treatment of 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-493 suppresses the proliferation and invasion of gastric cancer cells by targeting RhoC

Objective(s):MiRNAs have been proposed to be key regulators of tumorigenesis, progression and metastasis. However, their effect and prognostic value in gastric cancer is still poorly known. Materials and Methods: Gastric cancer cell lines were cultured. Tissue samples obtained from 36 gastric cancer patients were used for quantitative real-time PCR (qRT-PCR) analysis. The tissue microarrays (T...

متن کامل

Downregulation of TMEM40 by miR-138-5p suppresses cell proliferation and mobility in clear cell renal cell carcinoma

Background: Clear cell renal cell carcinoma (ccRCC) represents approximately 70% of RCC,as the most frequent histological subtype of RCC. MiR-138-5p, a tumor-related microRNA (miRNA), has been reported to be implicated in the diverse types of human malignancies, but its role in ccRCCremains unclear. Objective: The study was designed to investigate the function...

متن کامل

MicroRNA-124-3p inhibits cell growth and metastasis in cervical cancer by targeting IGF2BP1

MicroRNAs (miRs) serve a role in promoting and suppressing tumors in various types of malignant cancer, such as cervical cancer. However, the regulatory mechanism of miR-124-3p in cervical cancer remains unclear. In the present study, miR-124-3p was significantly downregulated in cervical cancer tissues and cell lines compared with matching adjacent non-tumor tissues and the normal cervical epi...

متن کامل

MicroRNA-454-3p inhibits cervical cancer cell invasion and migration by targeting c-Met

Increasing evidence has demonstrated that microRNAs (miRNAs) have a crucial role in the initiation and progression of tumors. The present study aimed to investigate the expression and the role of miRNA-454-3p in human cervical cancer. Human cervical cancer cells were transfected with miRNA-454-3p mimics or negative control miRNA. MTT, Transwell and wound healing assays were performed to investi...

متن کامل

LncRNA‐TCONS_00026907 is involved in the progression and prognosis of cervical cancer through inhibiting miR‐143‐5p

Our previous long noncoding RNA (lncRNA) microarray revealed that lncRNA-TCONS_00026907 is aberrantly expressed between cervical cancer tissues and adjacent tissues. This study aims to explore the potential role of TCONS_00026907 in the development of cervical cancer. The expression levels of TCONS_00026907 in cervical cancer tissues and adjacent tissues from 83 patients of cervical cancer were...

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 13  شماره 

صفحات  -

تاریخ انتشار 2017