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Anticancer activity of NOB1-targeted shRNA combination with TRAIL in epithelial ovarian cancer cells

Yang Lin1, Tianmin Xu1, Hong Teng1

  • 1Department of Obstetrics and Gynecology, The Second Hospital, Jilin University #218 Ziqiagn Street, Nanguan District, Changchun 130041, China.

International Journal of Clinical and Experimental Pathology
|December 1, 2015
PubMed

Insights

Combining NOB1 gene silencing with TRAIL therapy shows promise for ovarian cancer treatment. This combination enhances apoptosis and suppresses tumor growth by increasing DR5 expression and activating the MAPK pathway, overcoming TRAIL resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Therapy

Background:

  • Ovarian cancer treatment faces challenges due to tumor cell resistance to Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) therapy.
  • NOB1 (NIN1/RPN12 binding protein 1 homolog) downregulation via lentiviral short hairpin RNA (Lv/sh-NOB1) has previously shown potential in suppressing ovarian cancer growth.

Purpose of the Study:

  • To evaluate the synergistic effects of combining Lv/sh-NOB1 with TRAIL therapy against ovarian cancer.
  • To investigate the underlying mechanisms of this combination therapy in vitro and in vivo.

Main Methods:

  • In vitro experiments assessed proliferation, colony formation, apoptosis, and caspase activity (caspase-3, -8, -9) in ovarian cancer cells treated with Lv/sh-NOB1 and TRAIL.
  • In vivo studies utilized SKVO3 xenograft nude mice to evaluate the combination's effect on tumor growth.
  • Analysis of DR5 expression and MAPK pathway activation was performed.

Main Results:

  • The combination of Lv/sh-NOB1 and TRAIL synergistically inhibited ovarian cancer cell proliferation and colony formation.
  • Combined treatment significantly induced apoptosis and increased caspase activity in vitro.
  • In vivo, Lv/sh-NOB1 and TRAIL combination effectively suppressed tumor growth in a xenograft mouse model.
  • Downregulation of NOB1 led to increased DR5 expression and MAPK pathway activation, enhancing TRAIL sensitivity.

Conclusions:

  • The combination of Lv/sh-NOB1 and TRAIL represents a promising therapeutic strategy for ovarian cancer.
  • This approach overcomes TRAIL resistance by modulating DR5 expression and the MAPK pathway.
  • Further clinical investigation is warranted for this novel ovarian cancer treatment.
Keywords:
NOB1Ovarian cancerepithelial ovarian cancer

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