AI Article Synopsis
- CENPK is found to be significantly overexpressed in gastric cancer, correlating with poor patient prognosis.
- Knockdown experiments show that reducing CENPK levels inhibits cancer cell proliferation and promotes apoptosis, indicating a crucial role in tumor growth.
- The study identifies the PTEN-PI3K-AKT signaling pathway as a key mechanism by which CENPK influences gastric carcinogenesis, suggesting it could be a potential target for cancer treatment.
Article Abstract
Previous studies have indicated that centromere protein K (CENPK) is upregulated in several cancers and related to tumorigenesis. Nevertheless, the potential function of CENPK in gastric cancer (GC) remains unknown. Here, we investigated the function of CENPK on oncogenicity and explored its underlying mechanisms in GC. Our results showed that CENPK was dramatically overexpressed in GC and was associated with poor prognosis through bioinformatics analysis. We demonstrated that CENPK is upregulated in GC tissues and cell lines. Moreover, knockdown of CENPK significantly inhibited proliferation in vitro and attenuated the growth of implanted GCs in vivo. In addition, CENPK silencing induced G1 phase cell cycle arrest and facilitated apoptosis of GC cells. KEGG pathway analysis indicated that the PI3K-AKT signalling pathway was considerably enriched. Knockdown of CENPK decreased the expression of PI3K, p-Akt (Ser437) and p-GSK3β (Ser9) in GC cells, and increased the expression of PTEN. In conclusion, this study indicated that CENPK was overexpressed in GC and may promote gastric carcinogenesis through the PTEN-PI3K-AKT signalling pathway. Thus, CENPK may be a potential target for cancer therapeutics in GC.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8435434 | PMC |
| http://dx.doi.org/10.1111/jcmm.16850 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Centromere protein K enhances the activation of YAP1/TAZ signal cascade to drive the progression of clear cell renal cell carcinoma.
Toxicol Appl Pharmacol
January 2025
Department of Urinary Surgery, The Second Affiliated Hospital of Xi'an Jiaotong University, No. 157 Xiwu Road, Xi' an 710004, China. Electronic address:
Centromere protein K (CENPK) is a newly identified malignancy-related gene that exhibits differential expression in various cancers and plays a crucial role in carcinogenesis. However, it remains uncertain whether CENPK is involved in clear cell renal cell carcinoma (ccRCC). This work aimed to unveil the expression, clinical significance, biological functions, and regulatory mechanisms of CENPK in ccRCC.
View Article and Find Full Text PDFLentivirus-mediated short hairpin RNA interference of CENPK inhibits growth of colorectal cancer cells with overexpression of Cullin 4A.
World J Gastroenterol
October 2022
Department of Gastrointestinal Surgery, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010050, Inner Mongolia Autonomous Region, China.
Background: Colorectal cancer (CRC) is one of the most common malignant tumors worldwide. The identification of novel diagnostic and prognostic biomarkers for CRC is a key research imperative. Immunohistochemical analysis has revealed high expression of centromere protein K (CENPK) in CRC.
View Article and Find Full Text PDFThe cell cycle gene centromere protein K () contributes to the malignant progression and prognosis of prostate cancer.
Transl Cancer Res
May 2022
Department of Urology, Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Tianjin, China.
Background: The cell cycle gene centromere protein K () is upregulated in various cancers; however, the clinical value and mechanism of in prostate cancer (PCa) and castration-resistant prostate cancer (CRPC) remain unclear.
Methods: The expression of in PCa was analyzed in both patients with PCa and cell lines using immunohistochemistry (IHC), real-time quantitative reverse transcription PCR (qRT-PCR), Western blot and bioinformatics analyses. Knockdown of in PCa cells was achieved by transfecting siRNAs and assessed using qRT-PCR and Western blotting.
Knockdown of CENPK inhibits cell growth and facilitates apoptosis via PTEN-PI3K-AKT signalling pathway in gastric cancer.
J Cell Mol Med
September 2021
Department of Medical Oncology, Anhui Provincial Hospital, Hefei, Anhui, China.
Article Synopsis
- CENPK is found to be significantly overexpressed in gastric cancer, correlating with poor patient prognosis.
- Knockdown experiments show that reducing CENPK levels inhibits cancer cell proliferation and promotes apoptosis, indicating a crucial role in tumor growth.
- The study identifies the PTEN-PI3K-AKT signaling pathway as a key mechanism by which CENPK influences gastric carcinogenesis, suggesting it could be a potential target for cancer treatment.
Upregulation of centromere protein K is crucial for lung adenocarcinoma cell viability and invasion.
Adv Clin Exp Med
July 2021
Medical Laboratory, Second Affiliated Hospital of Mudanjiang Medical University, China.
Background: Identification of functional genes or biomarkers may be helpful for developing new treatment strategies in lung adenocarcinoma (LUAD). The centromere protein K (CENPK) gene has been discovered to be overexpressed and could influence tumor progression in several tumor types. However, its role in LUAD has never been revealed.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!