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SCARA5 inhibits oral squamous cell carcinoma via inactivating the STAT3 and PI3K/AKT signaling pathways

Juan Huang1, Chunhua Lv1, Baoyu Zhao1

  • 1Department of Stomatology, Taizhou People's Hospital, Tauzhou 225300, China.

Open Medicine (Warsaw, Poland)
|February 14, 2023
PubMed

Insights

Scavenger receptor class A member 5 (SCARA5) acts as a tumor suppressor in oral squamous cell carcinoma (OSCC). Overexpressing SCARA5 inhibits OSCC cell growth and induces apoptosis by impacting key signaling pathways.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Oral squamous cell carcinoma (OSCC) presents a significant global health challenge with high incidence and mortality rates.
  • Existing treatments necessitate novel therapeutic targets for improved patient outcomes.
  • Scavenger receptor class A member 5 (SCARA5) has been identified as a potential biomarker with reduced expression in OSCC.

Purpose of the Study:

  • To investigate the functional role of SCARA5 in OSCC.
  • To elucidate the molecular mechanisms underlying SCARA5's action in OSCC.

Main Methods:

  • Assessed SCARA5 expression in OSCC cell lines (CAL-27, SCC-9) versus normal oral keratinocytes.
  • Evaluated the effects of SCARA5 overexpression on cell proliferation, apoptosis, and epithelial-mesenchymal transition (EMT).
  • Analyzed the impact of SCARA5 on STAT3, PI3K, and AKT signaling pathway phosphorylation.

Main Results:

  • SCARA5 expression was significantly lower in OSCC cells compared to normal oral keratinocytes.
  • SCARA5 overexpression suppressed proliferation and induced apoptosis in OSCC cells.
  • SCARA5 repressed EMT by upregulating E-cadherin and downregulating N-cadherin.
  • SCARA5 inhibited the phosphorylation of STAT3, PI3K, and AKT signaling pathways.

Conclusions:

  • SCARA5 demonstrates a tumor suppressor role in OSCC.
  • SCARA5 inhibits OSCC cell proliferation and EMT while promoting apoptosis.
  • These effects are mediated through the suppression of STAT3 and PI3K/AKT signaling pathways.
Keywords:
OSCCPI3K/AKTSCARA5STAT3

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