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Peer-reviewedCC BY 4.0Frontiers in Oncology

PTPN1 downregulation contributes to pachymic acid-induced mitochondrial apoptosis in colorectal cancer cells

  • Chuang Liu1,2
  • Qiang Su1
  • Zhenxiang An1,2
  • Sufang Zhou1,2
  • Wen Che3
  1. 1The First Clinical Medical College, Guizhou University of Traditional Chinese Medicine
  2. 2Department of Gastroenterology, First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine
  3. 3Department of Pathology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine
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Abstract

Colorectal cancer (CRC) remains a major cause of cancer-related mortality. Pachymic acid (PA), a bioactive triterpenoid derived from Poria cocos, exhibits antitumor activity, but its effects on CRC and the involvement of PTPN1 remain unclear. This study investigated whether PTPN1 downregulation contributes to PA-induced mitochondrial apoptosis in HCT-116 CRC cells. Cell proliferation and migration were evaluated using viability, DNA synthesis, colony formation, wound healing, and transwell assays. Intracellular reactive oxygen species (ROS), mitochondrial membrane potential, apoptosis-related proteins, and the subcellular distribution of cytochrome c and Bax were examined. PTPN1 expression and overexpression rescue experiments were used to assess its functional involvement. PA inhibited cell proliferation and migration, increased ROS levels, and reduced mitochondrial membrane potential. These changes were accompanied by increased Bax, Bim, and cleaved caspase-3 expression, decreased Bcl-2 expression, and cytochrome c release from mitochondria into the cytoplasm. PA also downregulated PTPN1 expression. PTPN1 overexpression attenuated the effects of PA on proliferation, migration, ROS accumulation, mitochondrial membrane potential, and apoptosis-related protein expression. It also attenuated cytochrome c redistribution. These findings support a contribution of PTPN1 downregulation to PA-induced mitochondrial apoptosis in HCT-116 cells. Validation in additional CRC models, normal colonic epithelial cells, and in vivo systems is needed to establish the generalizability and therapeutic relevance of these findings.

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Cite

BibTeXRIS
BibTeX
@article{liu2026ptpn1,
  title = {{PTPN1 downregulation contributes to pachymic acid-induced mitochondrial apoptosis in colorectal cancer cells}},
  author = {Chuang Liu and Qiang Su and Zhenxiang An and Sufang Zhou and Wen Che},
  journal = {Frontiers in Oncology},
  year = {2026},
  month = oct,
  doi = {10.3389/fonc.2026.1891182},
  url = {https://www.frontiersin.org/articles/10.3389/fonc.2026.1891182/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - PTPN1 downregulation contributes to pachymic acid-induced mitochondrial apoptosis in colorectal cancer cells
AU  - Chuang Liu
AU  - Qiang Su
AU  - Zhenxiang An
AU  - Sufang Zhou
AU  - Wen Che
PY  - 2026
DA  - 2026/10/13
JO  - Frontiers in Oncology
DO  - 10.3389/fonc.2026.1891182
UR  - https://www.frontiersin.org/articles/10.3389/fonc.2026.1891182/full
AB  - Colorectal cancer (CRC) remains a major cause of cancer-related mortality. Pachymic acid (PA), a bioactive triterpenoid derived from Poria cocos, exhibits antitumor activity, but its effects on CRC and the involvement of PTPN1 remain unclear. This study investigated whether PTPN1 downregulation contributes to PA-induced mitochondrial apoptosis in HCT-116 CRC cells. Cell proliferation and migration were evaluated using viability, DNA synthesis, colony formation, wound healing, and transwell assays. Intracellular reactive oxygen species (ROS), mitochondrial membrane potential, apoptosis-related proteins, and the subcellular distribution of cytochrome c and Bax were examined. PTPN1 expression and overexpression rescue experiments were used to assess its functional involvement. PA inhibited cell proliferation and migration, increased ROS levels, and reduced mitochondrial membrane potential. These changes were accompanied by increased Bax, Bim, and cleaved caspase-3 expression, decreased Bcl-2 expression, and cytochrome c release from mitochondria into the cytoplasm. PA also downregulated PTPN1 expression. PTPN1 overexpression attenuated the effects of PA on proliferation, migration, ROS accumulation, mitochondrial membrane potential, and apoptosis-related protein expression. It also attenuated cytochrome c redistribution. These findings support a contribution of PTPN1 downregulation to PA-induced mitochondrial apoptosis in HCT-116 cells. Validation in additional CRC models, normal colonic epithelial cells, and in vivo systems is needed to establish the generalizability and therapeutic relevance of these findings.
SN  - 2234-943X
ER  -