CDKN2A inhibits cell proliferation and invasion in cervical cancer through LDHA-mediated AKT/mTOR pathway
1Department of Obstetrics and Gynecology, Zhongnan Hospital of Wuhan University, No. 169 Donghu Road, Wuchang District, Wuhan, 430071, Hubei, People's Republic of China.
Purpose:
The current study aims to explore the effects of CDKN2A on cell proliferation and cycle, and investigate the underlying mechanisms.
Methods:
Expression of CDKN2A in cervical cancer cell lines was evaluated by real-time quantitative PCR (RT-qPCR) and western blotting. Apoptotic rate was detected by Annexin V assay. MTT assay, Transwell assay and cell cycle assay kit were applied to examine the effect of CDKN2A on cell viability, invasion and cell cycle. Co-immunoprecipitation and western blotting were devoted to explore the mechanism by which CDKN2A contributes to cell function.
Results:
CDKN2A was expressed at a low level in cervical cancer cell lines. Overexpression of CDKN2A inhibited cell proliferation and invasion, and caused cell cycle arrest in the G1 phase. CDKN2A mediates the AKT-mTOR signaling pathway by suppressing lactate dehydrogenase (LDHA). Taken together, our data revealed that CDKN2A can be applied as a therapeutic target for the treatment of cervical cancer in future.
Conclusions:
CDKN2A inhibits cell proliferation and invasion in cervical cancer through LDHA-mediated AKT-mTOR pathway.
Insights
CDKN2A, a tumor suppressor, inhibits cervical cancer cell proliferation and invasion by regulating the LDHA-mediated AKT-mTOR pathway. This finding suggests CDKN2A as a potential therapeutic target for cervical cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Cervical cancer remains a significant global health challenge.
- Understanding the molecular mechanisms underlying cervical cancer progression is crucial for developing effective therapies.
Purpose of the Study:
- To investigate the role of CDKN2A in cervical cancer cell proliferation and cell cycle.
- To elucidate the underlying molecular mechanisms of CDKN2A's action in cervical cancer.
Main Methods:
- Gene expression analysis (RT-qPCR, Western blotting) of CDKN2A in cervical cancer cell lines.
- Assessment of apoptosis, cell viability, invasion, and cell cycle progression.
- Exploration of molecular mechanisms using co-immunoprecipitation and Western blotting.
Main Results:
- CDKN2A expression was found to be low in cervical cancer cell lines.
- Overexpression of CDKN2A significantly inhibited cell proliferation and invasion.
- CDKN2A induced cell cycle arrest at the G1 phase and mediated the AKT-mTOR signaling pathway by suppressing LDHA.
Conclusions:
- CDKN2A acts as a tumor suppressor in cervical cancer.
- CDKN2A inhibits proliferation and invasion via the LDHA-mediated AKT-mTOR pathway.
- CDKN2A presents a promising therapeutic target for cervical cancer treatment.
Related Concept Videos
Inhibition of Cdk Activity
M-Cdk Drives Transition Into Mitosis
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Positive Regulator Molecules
Positive Regulator Molecules
Anaphase Promoting Complex


