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Updated: Feb 6, 2026

Development of Compendium for Esophageal Squamous Cell Carcinoma
Published on: April 12, 2024
Karyopherin α2 induces apoptosis in tongue squamous cell carcinoma CAL-27 cells through the p53 pathway
Li Gao1, Lei Yu2, Chun-Ming Li1
1Department of Oral and Maxillofacial Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Abstract:
Tumor onset and progression are associated with dysfunction of the nuclear transport machinery at the level of import and export receptors. However, the role of Karyopherin α2 (KPNA2) in human tongue squamous cell carcinoma (TSCC) remains unknown. We assessed the proliferation, apoptosis and migration of TSCC CAL-27 cells using wound healing, Transwell and MTT assays, western blotting, electron microscopy and acridine orange/ethidium bromide staining following knockdown of KPNA2. The results revealed the antiproliferative, proapoptotic and anti-migratory effects of KPNA2 silencing on the TSCC CAL-27 cells. Moreover, the knockdown of KPNA2 proved to be accompanied by the upregulation of active caspase-3, cytochrome c, Bax, Bad and decreased expression of Bcl-2, p-Bad and XIAP. KPNA2 activated the caspase-dependent pathway in the CAL-27 cells with upregulation of p53, p21Cip1/Waf1 and p16INK4a. Thus, the present study demonstrated that p53/p21Cip1/Waf1/p16INK4a may be an important pathway involved in the function of KPNA2 in TSCC CAL-27 cells.
Insights
Karyopherin α2 (KPNA2) silencing inhibits human tongue squamous cell carcinoma (TSCC) cell proliferation and migration while promoting apoptosis. This suggests KPNA2 plays a key role in TSCC progression via the p53/p21Cip1/Waf1/p16INK4a pathway.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Nuclear transport is crucial for cell function; its dysfunction is linked to cancer.
- The specific role of Karyopherin α2 (KPNA2) in human tongue squamous cell carcinoma (TSCC) is currently unknown.
Purpose of the Study:
- To investigate the function of KPNA2 in TSCC.
- To determine the effects of KPNA2 knockdown on TSCC cell behavior and underlying molecular mechanisms.
Main Methods:
- TSCC CAL-27 cells were used to assess proliferation, apoptosis, and migration after KPNA2 knockdown.
- Techniques included wound healing, Transwell, MTT assays, western blotting, electron microscopy, and acridine orange/ethidium bromide staining.
Main Results:
- KPNA2 silencing demonstrated antiproliferative, proapoptotic, and anti-migratory effects on TSCC CAL-27 cells.
- Knockdown led to increased active caspase-3, cytochrome c, Bax, and Bad, with decreased Bcl-2, p-Bad, and XIAP.
- KPNA2 knockdown activated the caspase-dependent pathway and upregulated p53, p21Cip1/Waf1, and p16INK4a.
Conclusions:
- KPNA2 plays a significant role in the proliferation, apoptosis, and migration of TSCC cells.
- The p53/p21Cip1/Waf1/p16INK4a pathway is implicated in KPNA2's function in TSCC.
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