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CLEFMA Induces the Apoptosis of Oral Squamous Carcinoma Cells through the Regulation of the P38/HO-1 Signalling

Pei-Ni Chen1,2, Chiao-Wen Lin3,4, Shun-Fa Yang1,2

  • 1Institute of Medicine, Chung Shan Medical University, Taichung 402, Taiwan.

Cancers
|November 26, 2022
PubMed

Insights

CLEFMA effectively combats oral cancer by triggering apoptosis, a programmed cell death pathway. This occurs via the p38-dependent HO-1 signaling cascade, inhibiting tumor growth in both cell cultures and mouse models.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Oral Squamous Cell Carcinoma (OSCC) remains a significant global health challenge.
  • Identifying novel therapeutic agents with targeted mechanisms is crucial for improving patient outcomes.

Purpose of the Study:

  • To investigate the anti-tumour effects of CLEFMA in human OSCC.
  • To elucidate the molecular mechanisms underlying CLEFMA-induced cell death.

Main Methods:

  • In vitro assays: colony formation, flow cytometry, apoptosis array, Western blot, immunohistochemistry.
  • In vivo studies: SCC-9 xenograft mouse models treated with CLEFMA via oral gavage.
  • Molecular analysis: assessing HO-1, p38 MAPK, and caspase activation.

Main Results:

  • CLEFMA significantly inhibited colony formation and induced apoptosis in OSCC cell lines (HSC-3 and SCC-9).
  • CLEFMA treatment upregulated phosphorylated p38 and HO-1, alongside activating caspases (-3, -8, -9) and PARP cleavage.
  • HO-1 siRNA and p38 inhibitor (SB203580) attenuated CLEFMA-induced apoptosis, confirming the pathway's role.
  • In vivo, CLEFMA suppressed tumor growth in SCC-9 xenograft models.

Conclusions:

  • CLEFMA demonstrates potent anti-tumour activity against OSCC.
  • The mechanism involves CLEFMA-induced apoptosis mediated by the p38-MAPK/HO-1 signaling pathway.
  • CLEFMA represents a promising therapeutic candidate for oral cancer treatment.
Keywords:
CLEFMAHO-1apoptosisoral squamous carcinomap38

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