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TFE3 regulates renal adenocarcinoma cell proliferation via activation of the mTOR pathway

Yuan Fang1, Wei Bao2, Qiu Rao2

  • 1Reproductive Medical Center, Jinling Hospital, Clinical Medical School of Southern Medical University, Nanjing, Jiangsu 210002, P.R. China.

Molecular Medicine Reports
|July 18, 2017
PubMed

Insights

Transcription factor E3 (TFE3) overexpression enhances renal adenocarcinoma cell proliferation and colony formation. TFE3 may drive tumor growth by activating the mTOR signaling pathway and altering cell cycle progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Renal adenocarcinoma is a significant health concern.
  • The role of transcription factor E3 (TFE3) in renal cell proliferation requires further investigation.

Purpose of the Study:

  • To investigate the function of TFE3 in regulating renal adenocarcinoma cell proliferation.
  • To explore the underlying molecular mechanisms involving cell cycle and signaling pathways.

Main Methods:

  • Transfection of ACHN cells with lentivirus for TFE3 overexpression (OE) or negative control (NC).
  • Assays used include Western blot, MTT, plate colony formation, and flow cytometry.
  • Analysis of mammalian target of rapamycin (mTOR) and phosphorylated ribosomal protein S6 (p-rpS6) levels.

Main Results:

  • TFE3 overexpression significantly increased ACHN cell proliferation and colony formation.
  • Cell cycle analysis showed decreased G1/G2 phases and increased S phase in OE group.
  • Levels of mTOR and p-rpS6 were elevated in the TFE3 OE group.

Conclusions:

  • TFE3 overexpression promotes proliferation and colony formation in renal adenocarcinoma cells.
  • TFE3 may enhance renal tumor growth by modulating cell cycle progression.
  • Activation of the PI3K/AKT/mTOR pathway is implicated in TFE3-driven renal tumor growth.

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