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MAP7 interacts with RC3H1 and cooperatively regulate cell-cycle progression of cervical cancer cells via activating

Rong Zhang1, Lei Li2, Lingli Chen3

  • 1Department of Gynecology and Obstetrics, Tianjin Medical University General Hospital, Tianjin, 300052, China; Department of Gynecology and Obstetrics, People's Hospital of Shanxi Province, Taiyuan, 030012, China.

Biochemical and Biophysical Research Communications
|May 25, 2020
PubMed

Insights

Microtubule-associated protein MAP7 and RC3H1 interact to drive cervical cancer cell cycle progression. This interaction elevates cyclin D1/B1 and activates IKK/NF-kB signaling, impacting patient survival.

Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Biology

Background:

  • Ensconsin, encoded by the MAP7 gene, is a microtubule-associated protein implicated in cellular functions.
  • Cervical cancer progression involves dysregulation of cell-cycle control mechanisms.
  • Understanding novel protein interactions is crucial for identifying therapeutic targets in cervical cancer.

Purpose of the Study:

  • To investigate the functional roles and interaction partners of MAP7 in cervical cancer cell-cycle progression.
  • To explore the potential of MAP7 as a biomarker for patient survival.
  • To elucidate the molecular mechanisms underlying MAP7's function in cervical cancer.

Main Methods:

  • Bioinformatic analysis of TCGA-CESC and GTEx datasets for MAP7 expression and correlation with survival.
  • In vitro and in vivo studies using SiHa cervical cancer cells.
  • Co-immunoprecipitation (Co-IP) assays to identify MAP7 interacting proteins.
  • Gene knockdown experiments and Western blotting to assess protein expression and signaling pathway activation (IKK/NF-kB).

Main Results:

  • MAP7 mRNA expression is an independent biomarker associated with shorter survival in cervical cancer patients.
  • MAP7 overexpression enhances cyclin D1/B1 levels, promotes cell-cycle progression, and tumor growth in vivo.
  • A novel interaction between MAP7 and RC3H1 was confirmed; their coordinated action is essential for cyclin D1/B1 upregulation and cell-cycle promotion.
  • MAP7-induced cell-cycle progression is mediated by the activation of canonical IKK/NF-kB signaling, involving increased P-IKK and P-p65 expression.
  • MAP7 expression is regulated by copy number variations and DNA methylation, with demethylation enhancing its expression.

Conclusions:

  • MAP7 and RC3H1 form a novel functional complex in cervical cancer cells that cooperatively drives cell-cycle progression.
  • This interaction promotes cyclin D1/B1 expression and activates the IKK/NF-kB pathway, contributing to tumor growth.
  • MAP7 serves as a potential prognostic biomarker and therapeutic target in cervical cancer.
Keywords:
Cell-cycleCervical cancerMAP7NF-κB signalingRC3H1

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