Skip to main content

Open Access Tumor-Suppressor Gene NBPF1 Inhibits Invasion and PI3K/mTOR Signaling in Cervical Cancer Cells

The purpose of this study was to assess the effects of NBPF1 expression on cervical cancer cell invasion and apoptosis and to illustrate its potential mechanism. Human cervical cancer HeLa cells were transfected with the constructed siNBPF1 or pcDNA3.1-NBPF1 vectors. Effects of NBPF1 expression on cell invasion ability and cell apoptosis were analyzed using the Matrigel method and an Annexin V-FITC cell apoptosis kit, respectively. In addition, cell apoptosis-related proteins involved with the PI3K/mTOR signaling pathway were analyzed using Western blot. Remediation experiments were conducted to verify the effects of NBPF1 expression on cell invasion and apoptosis. Compared to the control, mRNA and protein expressions of NBPF1 were significantly decreased when cells were transfected with siNBPF1 (p < 0.05), which was contrary to the results of cells transfected with pcDNA3.1-NBPF1. Overexpression of NBPF1 significantly suppressed HeLa cell invasion but promoted cell apoptosis (p < 0.05). Overexpression of NBPF1 performed a significant inhibitory role on PI3K/mTOR signal pathway expression, while NBPF1 was silenced, showing contrary results. Our data suggested that NBPF1 overexpression may be a suppressor for cervical cancer via affecting cell invasion and apoptosis through regulating PI3K/mTOR signaling pathway. NBPF1 may be a potential therapeutic target for cervical cancer treatment.

Keywords: Cell apoptosis; Cell invasion; Cervical cancer; Neuroblastoma breakpoint family member 1 (NBPF1); PI3K/mTOR pathway

Document Type: Research Article

Affiliations: Department of Obstetrics and Gynecology, AnKang City Central Hospital, Shanxi, China

Publication date: 21 January 2016

More about this publication?
  • Formerly: Oncology Research Incorporating Anti-Cancer Drug Design
    Oncology Research Featuring Preclinical and Clincal Cancer Therapeutics publishes research of the highest quality that contributes to an understanding of cancer in areas of molecular biology, cell biology, biochemistry, biophysics, genetics, biology, endocrinology, and immunology, as well as studies on the mechanism of action of carcinogens and therapeutic agents, reports dealing with cancer prevention and epidemiology, and clinical trials delineating effective new therapeutic regimens.

    From Volume 23, Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics is Open Access under the terms of the Creative Commons CC BY-NC-ND license.

  • Editorial Board
  • Information for Authors
  • Submit a Paper
  • Ingenta Connect is not responsible for the content or availability of external websites
  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content