Upregulation of CENPM promotes hepatocarcinogenesis through mutiple mechanisms

Xiao, Yusha; Najeeb, Rahmathullah Mohamed; Ma, Dong; Yang, Kang; Zhong, Qi; Liu, Quanyan

doi:10.1186/s13046-019-1444-0

Cited by 52 publications

(39 citation statements)

References 43 publications

(49 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recently, Yu et al defined CENPM as a complement to AFP in the diagnosis of hepatocellular carcinoma ( 8 ); Xiao et al further confirmed that CENPM was highly associated with hepatocellular carcinoma progression and could be a candidate novel biomarker for hepatocellular carcinoma ( 28 ). Investigations of the underlying mechanisms of melanoma highlighted that CENPM may play an important role in the metastases of melanoma ( 9 ).…”

Section: Discussionmentioning

confidence: 99%

Upregulation of CENPM facilitates tumor metastasis via the mTOR/p70S6K signaling pathway in pancreatic cancer

et al. 2020

View full text Add to dashboard Cite

Pancreatic cancer is a severe disease with high morbidity and mortality. However, the primary molecular mechanisms of pancreatic tumor formation and progression remain unclear. The present study using sequencing technology revealed that the centromere protein M (CENPM) gene was overexpressed in pancreatic cancer tissues. CENPM is one of the components of a complex that plays a central role in kinetochore protein assembly, mitotic progression and chromosome segregation. However, the biological function of CENPM in pancreatic cancer has yet to be determined. Hence, two effective siRNAs were designed to knock down CENPM. Notably, downregulation of CENPM inhibited pancreatic cancer cell proliferation, altered the cell cycle and limited pancreatic cancer cell migration and invasion via the mTOR/p70S6K signaling pathway. This research provides new evidence that CENPM overexpression plays a significant role in the progression of pancreatic cancer. Overall, the present findings indicated that CENPM may be a significant biomarker for predicting the development and progression of pancreatic malignancy.

show abstract

Section: Discussionmentioning

confidence: 99%

Upregulation of CENPM facilitates tumor metastasis via the mTOR/p70S6K signaling pathway in pancreatic cancer

et al. 2020

View full text Add to dashboard Cite

show abstract

“…It was found that 5 genes, including NUDT1 , E2F1 , CCNE2 , MCM5 , and CENPM , had significant correlation indices with CDC45 and were upregulated in HCC tissues. Numerous studies agree that the increased expression of these 5 genes is associated with a poor prognosis and more advanced tumor stages in HCC patients [ 13 , 26 – 30 ]. Moreover, research showed that E2F1 regulates DNAJA1 to promote cell proliferation and metastasis by stabilizing CDC45 in colorectal cancer cell lines [ 21 ] and that silencing CCNE2 or CENPM could inhibit HCC cell growth [ 30 , 31 ].…”

Section: Discussionmentioning

confidence: 99%

Expression of Cell Division Cycle Protein 45 in Tissue Microarrays and the CDC45 Gene by Bioinformatics Analysis in Human Hepatocellular Carcinoma and Patient Outcomes

et al. 2020

Med Sci Monit

View full text Add to dashboard Cite

Background Hepatocellular carcinoma (HCC) causes a heavy disease burden worldwide. Cell division cycle 45 (Cdc45) and its encoding gene ( CDC45 ) have been studied for a long time, but their expression patterns and roles in liver carcinogenesis and advanced HCC deterioration are still incompletely understood. This study integrated tissue microarray and bioinformatics analyses to explore the expression and clinical value of CDC45 and Cdc45 in HCC. Material/Methods In HCC, the expression and relationships with clinic-pathological parameters of CDC45 and Cdc45 were investigated by integrating the RNA-sequencing data, downloaded from The Cancer Genome Atlas and Oncomine databases, and tissue microarray with immunohistochemistry staining. Co-expressed genes and genetic alterations of CDC45 separately obtained from Oncomine and cBioPortal databases were identified to shed light on the potential mechanisms of CDC45 in HCC. Results CDC45 and Cdc45 were both overexpressed in HCC tissues, and the CDC45 level progressively increased from stage I to III. The survival outcomes of the group with high CDC45 expression were significantly worse compared with the group with low expression. Amplification and deep deletion were 2 major significant alteration types in HCC patients, and the outcomes were worse in patients with altered versus unaltered CDC45 . NUDT1 , E2F1 , CCNE2 , MCM5 , and CENPM were identified as the most significantly co-expressed genes. Conclusions CDC45 and Cdc45 were both upregulated in HCC, and increased expression levels and genetic alternations of CDC45 were correlated with worse prognosis in HCC patients. CDC45 may promote HCC by co-expressing with NUDT1 , E2F1 , CCNE2 , MCM5 , and CENPM .

show abstract

“…The aberrant expression of miR-497-5p plays an essential role in tumorigenesis. miR-497-5p has been proven to be downregulated in NSCLC, gastric cancer, colorectal cancer, ovarian cancer, renal cell carcinoma, and melanoma [88][89][90][91][92][93][94][95]. Furthermore, in vitro and in vivo studies revealed that miR-497-5p overexpression suppressed HCC cell proliferation, colony formation, and metastasis [96].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-497-5p Is Downregulated in Hepatocellular Carcinoma and Associated with Tumorigenesis and Poor Prognosis in Patients

Jiang

Liu

et al. 2021

International Journal of Genomics

View full text Add to dashboard Cite

Background. MicroRNAs (miRNAs) have been demonstrated to exhibit important regulatory roles in multiple malignancies, including hepatocellular carcinoma (HCC). hsa-miR-497-5p was reported to involve in cancer progression and poor prognosis in many kinds of tumors. However, the expression and its clinical significance of hsa-miR-497-5p in HCC remain unclear. Methods. In the present study, we investigated the expression of hsa-miR-497-5p in HCC and analyzed the correction of clinical features with prognosis. The expression levels of hsa-miR-497-5p and potential target genes were analyzed in HCC and adjacent noncancerous tissues using The Cancer Genome Atlas (TCGA) database and Gene Expression Omnibus (GEO) datasets. Real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to analyze hsa-miR-497-5p levels in 328 HCC tissues and 30 paired adjacent noncancer tissues. Overall survival (OS) and progression-free survival (PFS) of patients with HCC were assessed using the Kaplan-Meier method and the log-rank test. Results. The hsa-miR-497-5p expression levels were decreased, and its target genes ACTG1, CSNK1D, PPP1CC, and BIRC5 were upregulated in HCC tissues compared with normal tissues. Lower levels of hsa-miR-497-5p expression and higher levels of the four target genes were significantly associated with higher tumor diameter. Moreover, patients with lower hsa-miR-497-5p expression and higher target genes levels had shorter OS. Conclusion. The expression levels of hsa-miR-497-5p may play an important regulatory role in HCC and are closely correlated with HCC progression and poor prognosis in patients. The hsa-miR-497-5p may be a specific therapeutic target for the treatment of HCC.

show abstract

Upregulation of CENPM promotes hepatocarcinogenesis through mutiple mechanisms

Cited by 52 publications

References 43 publications

Upregulation of CENPM facilitates tumor metastasis via the mTOR/p70S6K signaling pathway in pancreatic cancer

Upregulation of CENPM facilitates tumor metastasis via the mTOR/p70S6K signaling pathway in pancreatic cancer

Expression of Cell Division Cycle Protein 45 in Tissue Microarrays and the CDC45 Gene by Bioinformatics Analysis in Human Hepatocellular Carcinoma and Patient Outcomes

MicroRNA-497-5p Is Downregulated in Hepatocellular Carcinoma and Associated with Tumorigenesis and Poor Prognosis in Patients

Contact Info

Product

Resources

About