Prognostic Relevance of HJURP Expression in Patients with Surgically Resected Colorectal Cancer

Kang, Dong Hyun; Woo, Jongsoo; Kim, Hyeongjoo; Kim, Soo Youn; Ji, Sanghee; Jaygal, Gunn; Ahn, Tae Sung; Kim, Hee Jin; Kwak, Hyoung Jong; Kim, Chang‐Jin; Baek, Moo Jun; Jeong, Dongjun

doi:10.3390/ijms21217928

Cited by 31 publications

(27 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, in hepatocellular carcinoma 12 , 26 , HJURP is also stained in the cytoplasm. However, in pancreatic cancer 27 and colorectal cancer 28 , its localization is mainly in the nucleus. In glioma 29 , HJURP is stained in both cytoplasm and nucleus.…”

Section: Discussionmentioning

confidence: 99%

HJURP promotes proliferation in prostate cancer cells through increasing CDKN1A degradation via the GSK3β/JNK signaling pathway

et al. 2021

View full text Add to dashboard Cite

Genes with cross-cancer aberrations are most likely to be functional genes or potential therapeutic targets. Here, we found a total of 137 genes were ectopically expressed in eight cancer types, of which Holliday junction recognition protein (HJURP) was significantly upregulated in prostate cancer (PCa). Moreover, patients with higher HJURP mRNA and protein levels had poorer outcomes, and the protein levels served as an independent prognosis factor for the overall survival of PCa patients. Functionally, ectopic HJURP expression promoted PCa cells proliferation in vitro and in vivo. Mechanistically, HJURP increased the ubiquitination of cyclin-dependent kinase inhibitor 1 (CDKN1A) via the GSK3β/JNK signaling pathway and decreased its stability. This study investigated the role of HJURP in PCa proliferation and may provide a novel prognostic and therapeutic target for PCa.

show abstract

Section: Discussionmentioning

confidence: 99%

HJURP promotes proliferation in prostate cancer cells through increasing CDKN1A degradation via the GSK3β/JNK signaling pathway

et al. 2021

View full text Add to dashboard Cite

show abstract

“…In a study by M Miyo, the proliferation of SW480 cells was reduced compared with HCT116 cells, but the migration capacity was increased [ 53 ]. In another study, the proliferation of SW620 and SW480 cells was lower than that of HCT116 and HT29 cells, but the migration and invasion abilities were increased compared with HCT116 and HT29 cells [ 54 ]. These findings indicated that different tumour cell lines may have different proliferation and tumourigenesis mechanisms, which may partially be explained by the enrichment and loss of biological phenotypes in the process of establishing different cell lines and might also be related to the different donor sources.…”

Section: Discussionmentioning

confidence: 99%

Claudin-7 deficiency promotes stemness properties in colorectal cancer through Sox9-mediated Wnt/β-catenin signalling

Ding

Wang

et al. 2021

J Transl Med

View full text Add to dashboard Cite

Background Colorectal cancer (CRC) is a common malignant tumour of the digestive tract that is characterized by high patient morbidity and mortality rates. Claudin-7 (Cldn7), a tight junction protein, was recently reported to function as a candidate tumour suppressor gene in CRC. Our previous study demonstrated that the large intestine of C57/BL6 mice showed intestinal adenomas and abnormal Ki67 expression and distribution in the intestinal crypt when Cldn7 was knocked out. The aim of this study was to further investigate whether Cldn7 deficiency has non-tight junction functions, affects intestinal stemness properties, promotes CRC and to determine the specific mechanism. Methods Cell proliferation assays, migration assays, apoptosis assays, tumour sphere formation assays in vitro, and subcutaneous xenograft models in vivo were used to determine the effects of Cldn7 knockdown on the biological characteristics of CRC stem cells. Western blotting, qPCR and immunofluorescence staining were performed to identify the epithelial-mesenchymal transition and the activation of Wnt/β-catenin pathway in CRC stem cells. Cldn7 inducible conditional gene knockout mice and immunohistochemical staining further verified this hypothesis in vivo. The mechanism and target of Cldn7 were determined by performing a chromatin immunoprecipitation (ChIP) assay and coimmunoprecipitation (CoIP) assay. Results Cldn7 knock down in CRC stem cells promoted cell proliferation, migration, and globular growth in serum-free medium and the ability to form xenograft tumours; cell apoptosis was inhibited, while the cellular epithelial-mesenchymal transition was also observed. These changes in cell characteristics were achieved by activating the Wnt/β-catenin pathway and promoting the expression of downstream target genes after β-catenin entry into the nucleus, as observed in CRC cell lines and Cldn7 gene knockout mouse experiments. Using ChIP and CoIP experiments, we initially found that Cldn7 and Sox9 interacted at the protein level to activate the Wnt/β-catenin pathway. Conclusions Based on our research, Cldn7 deficiency confers stemness properties in CRC through Sox9-mediated Wnt/β-catenin signalling. This result clarifies that Cldn7 plays an inhibitory role in CRC and reveals a possible molecular mechanism, which is conducive to further research on Cldn7 and cancer stem cells.

show abstract

“…HJURP knockdown suppressed the migration and invasion of NSCLC cells via inhibition of the activation of Wnt/β-catenin signaling ( Wei et al, 2019 ). Similarly, ectopic expression of HJURP can promote proliferation, migration, and invasion of other tumor cells ( Chen T. et al, 2018 , 2019 ; Kang et al, 2020 ). Furthermore, high expression of HJURP is associated with poor prognosis in patients with colorectal and ovarian cancer and is an independent prognostic biomarker for those cancers ( Li et al, 2018 ; Kang et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Construction of a circRNA-Related Prognostic Risk Score Model for Predicting the Immune Landscape of Lung Adenocarcinoma

Wang

Zhang

2021

Front. Genet.

View full text Add to dashboard Cite

The purpose of this study was to construct a circular RNA (circRNA)-related competing endogenous RNA (ceRNA) regulatory network and risk score model for lung adenocarcinoma (LUAD). The relationship of the risk score to immune landscape and sensitivity to chemotherapy and targeted therapy of LUAD was assessed. We downloaded mRNA and miRNA expression data, along with clinical information, from The Cancer Genome Atlas (TCGA) program, and circRNA expression data from the Gene Expression Omnibus (GEO) database and identified differently expressed circRNA (DEcircRNA), miRNA (DEmiRNA), and mRNA (DEmRNA) using R software. We then constructed the circRNA-related network using bioinformatics method. The risk score model was established by LASSO Cox regression analysis based on 10 hub genes. In addition, the risk score model was an independent predictor for overall survival (OS) in both the TCGA and CPTAC datasets. Patients in the high-risk group had shorter OS and disease-free survival (DFS) than those in the low-risk group and were more sensitive to chemotherapy and targeted therapy. The types of tumor-infiltrating immune cells were different in the high- and low-risk groups. Our data revealed that the circRNA-related risk score model is closely associated with the level of immune cell infiltration in the tumor and the effects of adjuvant treatment. This network may be useful in designing personalized treatments for LUAD patients.

show abstract

Prognostic Relevance of HJURP Expression in Patients with Surgically Resected Colorectal Cancer

Cited by 31 publications

References 21 publications

HJURP promotes proliferation in prostate cancer cells through increasing CDKN1A degradation via the GSK3β/JNK signaling pathway

HJURP promotes proliferation in prostate cancer cells through increasing CDKN1A degradation via the GSK3β/JNK signaling pathway

Claudin-7 deficiency promotes stemness properties in colorectal cancer through Sox9-mediated Wnt/β-catenin signalling

Construction of a circRNA-Related Prognostic Risk Score Model for Predicting the Immune Landscape of Lung Adenocarcinoma

Contact Info

Product

Resources

About