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KMT2A regulates cervical cancer cell growth through targeting VDAC1

Changlin Zhang1, Yijun Hua2, Huijuan Qiu2

  • 1Department of Gynecology, The Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, China.

Aging
|May 22, 2020
PubMed

Insights

The KMT2A/VDAC1 signaling axis drives cervical cancer progression. Inhibiting KMT2A or VDAC1 suppressed tumor growth, proliferation, and migration, offering potential therapeutic targets for cervical cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Cervical cancer requires new therapeutic targets.
  • KMT2A's role in cervical cancer is unexplored.
  • KMT2A is a known transcriptional co-activator.

Purpose of the Study:

  • Investigate KMT2A's function in cervical cancer.
  • Determine if KMT2A targets VDAC1 in cervical cancer.
  • Explore the KMT2A/VDAC1 axis as a therapeutic target.

Main Methods:

  • KMT2A knockdown and overexpression in cervical cancer cells.
  • Analysis of cell proliferation, migration, and apoptosis.
  • In vivo studies using a cervical cancer xenograft mouse model.
  • Examination of clinical cervical cancer samples and databases.

Main Results:

  • KMT2A knockdown inhibited cervical cancer cell proliferation, migration, and induced apoptosis via the PARP/caspase pathway and VDAC1 inhibition.
  • VDAC1 overexpression counteracted KMT2A knockdown effects.
  • KMT2A knockdown suppressed tumor growth in vivo, while KMT2A overexpression promoted it.
  • KMT2A and VDAC1 were upregulated in cervical squamous cell carcinoma and negatively correlated with differentiation.

Conclusions:

  • The KMT2A/VDAC1 signaling axis is implicated in cervical carcinogenesis.
  • KMT2A and VDAC1 represent potential therapeutic targets for cervical cancer treatment.
Keywords:
KMT2AVDAC1cervical cancer

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