THUMPD3-AS1 inhibits ovarian cancer cell apoptosis through the miR-320d/ARF1 axis

Qingling Mu1, Xin Wang1, Kui Huang2

  • 1Department of Gynecology and Obstetrics, Qingdao Municipal Hospital, Qingdao, Shandong, China.

Insights

THUMPD3-AS1 promotes ovarian cancer by sponging miR-320d, leading to increased ARF1 and reduced apoptosis. Targeting this long noncoding RNA (lncRNA) pathway offers a potential therapeutic strategy for ovarian cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Ovarian cancer is a prevalent gynecologic malignancy with a poor prognosis.
  • Long noncoding RNAs (lncRNAs) like THUMPD3-AS1 are implicated as oncogenes in various cancers.
  • Dysregulation of miR-320d and ARF1 is observed in ovarian cancer, but the role of THUMPD3-AS1 remains unclear.

Purpose of the Study:

  • To elucidate the role of THUMPD3-AS1 in ovarian cancer.
  • To investigate the underlying molecular mechanism involving miR-320d and ARF1.
  • To assess THUMPD3-AS1 as a potential therapeutic target for ovarian cancer.

Main Methods:

  • In vitro experiments using human ovarian epithelial and cancer cell lines.
  • Assays for cell viability (CCK-8), apoptosis (flow cytometry, TUNEL), and protein/mRNA levels (Western blot, RT-qPCR).
  • Dual luciferase assay to validate targeting relationships between THUMPD3-AS1, miR-320d, and ARF1.

Main Results:

  • THUMPD3-AS1 and ARF1 were highly expressed, while miR-320d was lowly expressed in ovarian cancer cells.
  • THUMPD3-AS1 knockdown suppressed cell viability and induced apoptosis.
  • THUMPD3-AS1 acts as a miR-320d sponge, upregulating ARF1 and inhibiting apoptosis.

Conclusions:

  • THUMPD3-AS1 promotes ovarian cancer progression by modulating the miR-320d/ARF1 axis.
  • The THUMPD3-AS1/miR-320d/ARF1 pathway is a potential therapeutic target for ovarian cancer treatment.

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