DEPDC1B knockdown inhibits the development of malignant melanoma through suppressing cell proliferation and inducing cell apoptosis

Exp Cell Res. 2019 Jun 1;379(1):48-54. doi: 10.1016/j.yexcr.2019.03.021. Epub 2019 Mar 14.

Abstract

Malignant melanoma (MM) remains the leading cause of skin cancer related death, which has very poor prognosis because of locoregional recurrence and distant metastasis. DEPDC1B (DEP domain-containing protein 1B), has been proved to be associated with some types of malignant tumors. However, the role of DEPDC1B in MM is still unknown. In this study, the expression levels of DEPDC1B in MM tissues were detected by IHC. DEPDC1B knockdown cell lines were constructed, evaluated by Western blot and qRT-PCR, and also used for construction of mice xenograft models. Cell proliferation and apoptosis were investigated by MTT, colony formation assay and flow cytometry, respectively. The results indicated significantly up-regulated expression of DEPDC1B in tumor tissues. Moreover, knockdown of DEPDC1B could inhibit cell proliferation while inducing cell apoptosis. The in vivo study demonstrated the significant suppression of tumor growth by knockdown of DEPDC1B. Finally, the results of antibody array proved the up-regulation of pro-apoptotic proteins and the down-regulation of anti-apoptotic proteins by DEPDC1B knockdown. Therefore, it could be concluded that DEPDC1B was involved in the development and progression of MM, which may act as promotor for MM and could be a potential therapeutic target.

Keywords: Cell apoptosis; Cell proliferation; DEPDC1B; Knockdown; Malignant melanoma.

MeSH terms

  • Animals
  • Apoptosis / genetics*
  • Cell Death / genetics
  • Cell Line, Tumor
  • Cell Proliferation / genetics*
  • Down-Regulation / genetics
  • GTPase-Activating Proteins / genetics*
  • Gene Expression Regulation, Neoplastic / genetics
  • Humans
  • Male
  • Melanoma / genetics*
  • Melanoma / pathology
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • Prognosis
  • Skin Neoplasms / genetics
  • Skin Neoplasms / pathology
  • Up-Regulation / genetics
  • Xenograft Model Antitumor Assays / methods

Substances

  • DEPDC1B protein, human
  • GTPase-Activating Proteins