TRPM7 is overexpressed in bladder cancer and promotes proliferation, migration, invasion and tumor growth

نویسندگان

  • Sheng-Lin Gao
  • Chui-Ze Kong
  • Zhe Zhang
  • Ze-Liang Li
  • Jian-Bin Bi
  • Xian-Kui Liu
چکیده

Recent findings suggest that the melastatin transient receptor potential channel 7 (TRPM7) is overexpressed in many types of cancers and is involved in tumorigenesis. However, its expression pattern and the potential role in bladder cancer remain unclear. The aim of the present study was to investigate the expression status of TRPM7 and its relationship with the development of bladder cancer. In the present study, we observed that the expression of TRPM7 was significantly elevated in bladder cancer tissues compared with that noted in the adjacent non-tumor tissues. Furthermore, increased TRPM7 expression was significantly associated with recurrence, metastasis and prognosis. In addition, after knockdown of the expression of TRPM7 by siRNA, the proliferation and the motility of T24 and 5637 cells were obviously inhibited, and downregulation of TRPM7 was found to play an important role in bladder cancer cell apoptosis. In conclusion, our findings suggest that TRPM7 plays an important role in bladder cancer, and TRPM7 may serve as a potentially unfavorable factor and novel target for human bladder cancer.

برای دانلود رایگان 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-6165 Dysregulation in Breast Cancer and Its Effect on Cell Proliferation and Migration

Background: ncRNAs have been identified as oncogenic drivers and tumor suppressors in any type of cancer. Although many classes of ncRNAs have been reported, most studies have been performed on microRNAs (miRNAs). miRNAs can regulate several target genes and affect important processes such as homeostasis, angiogenesis, cell proliferation, differentiation, and apoptosis. Located in the p75NTR ge...

متن کامل

Role of TRPM7 in Cancer: Potential as Molecular Biomarker and Therapeutic Target

The transient receptor potential melastatin-subfamily member 7 (TRPM7) is a ubiquitously expressed ion channel with intrinsic kinase activity. Molecular and electrophysiological analyses of the structure and activity of TRPM7 have revealed functional coupling of its channel and kinase activity. Studies have indicated the important roles of TRPM7 channel-kinase in fundamental cellular processes,...

متن کامل

Long Non-coding RNA ZEB1-AS1 Promotes Tumorigenesis and Metastasis in Colorectal Cancer

Emerging evidence implicates that a large fraction of human genome was transcribed but the transcripts known as long non coding RNA are not translated into proteins. They are contributing in different cellular processes, including cellular proliferation and apoptosis. LncRNAs were found to play critical roles in many diseases and act as key regulators in malignancies. In this study, we investig...

متن کامل

P157: Periostin Recruits Tumor Associated Macrophages in Glioblastoma Multiform

Glioblastoma multiform (GBM) is the most common and lethal type of primary brain tumors with high rates of morbidity and mortality. Treatment options are limited and ineffective in most of the cases. Epidemiological studies have shown a link between inflammation and glioma genesis.  In addition, at the molecular level, pro-inflammatory cytokines released from activated microglia can increa...

متن کامل

Long non-coding RNA FOXO1 inhibits lung cancer cell growth through down-regulating PI3K/AKT signaling pathway

Objective(s): Lung cancer is one of the most common malignant tumors, which seriously threatens the health and life of the people. Recently, a novel long non-coding RNA (lncRNA) termed lncFOXO1 was found and investigated in breast cancer. However, the effect of lncFOXO1 on lung cancer is still ambiguous. The current study aimed to uncover the functions of lncFOXO1 in l...

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

عنوان ژورنال:

دوره 38  شماره 

صفحات  -

تاریخ انتشار 2017