KIF14 and KIF23 Promote Cell Proliferation and Chemoresistance in HCC Cells, and Predict Worse Prognosis of Patients with HCC

Cheng, Chunxia; Wu, Xingxing; Shen, Yun; Li, Quanxi

doi:10.2147/cmar.s285367

Cited by 23 publications

(24 citation statements)

References 52 publications

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“…RRM2 promotes the occurrence of cell resistance by activating the EGFR/AKT pathway, while lncRNA can up-regulate RRM2 by binding to and inhibiting the expression of miR-139-5p, which is consistent with our research [50]. KIF23 is related to the worse prognosis of HCC patients and has a promoting effect on the proliferation and chemoresistance of HCC cells [51]. TXNIP has long been recognized as a potential tumor suppressor gene that inhibits cell growth and is involved in stress response, REDOX regulation, and cell proliferation [52,53].…”

Section: Plos Onesupporting

confidence: 91%

Tumor infiltrating lymphocytes associated competitive endogenous RNA networks as predictors of outcome in hepatic carcinoma based on WGCNA analysis

Rui

Peng

et al. 2021

PLoS ONE

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Background The important regulatory role of competitive endogenous RNAs (ceRNAs) in hepatocellular carcinoma (HCC) has been confirmed. Tumor infiltrating lymphocytes (TILs) are of great significance to tumor outcome and prognosis. This study will systematically analyze the key factors affecting the prognosis of HCC from the perspective of ceRNA and TILs. Methods The Cancer Genome Atlas (TCGA) database was used for transcriptome data acquisition of HCC. Through the analysis of the Weighted Gene Co-expression Network Analysis (WCGNA), the two modules for co-expression of the disease were determined, and a ceRNA network was constructed. We used Cox regression and LASSO regression analysis to screen prognostic factors and constructed a risk score model. The Gene Expression Omnibus (GEO) was used to validate the model. The Kyoto Encyclopedia of Genes and Genomes (KEGG) was used for mRNAs functional analysis. The cell composition of TILs was analyzed by the CIBERSORT algorithm, and Pearson correlation analysis was utilized to explore the correlation between TILs and prognostic factors. Results We constructed a ceRNA regulatory network composed of 67 nodes through WGCNA, including 44 DElncRNAs, 19 DEGs, and 4 DEmiRNAs. And based on the expression of 4 DEGs in this network (RRM2, LDLR, TXNIP, and KIF23), a prognostic model of HCC with good specificity and sensitivity was developed. CIBERSORT analyzed the composition of TILs in HCC tumor tissues. Correlation analysis showed that RRM2 is significantly correlated with T cells CD4 memory activated, T cells CD4 memory resting, T cells CD8, and T cells follicular helper, and TXNIP is negatively correlated with B cells memory. Conclusions In this study, a ceRNA with prognostic value in HCC was created, and a prognostic risk model for HCC was constructed based on it. This risk score model is closely related to TILs and is expected to become a potential therapeutic target and a new predictive indicator.

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Section: Plos Onesupporting

confidence: 91%

Tumor infiltrating lymphocytes associated competitive endogenous RNA networks as predictors of outcome in hepatic carcinoma based on WGCNA analysis

Rui

Peng

et al. 2021

PLoS ONE

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“…Recently, accumulating studies focused on the molecular mechanisms of cisplatin chemoresistance emerged. For example, the kinesin superfamily (KIF) members KIF14 and KIF23 have been shown to promote cisplatin-resistance in HCC (Cheng et al, 2020). Branched-chain amino acid transaminase 1 (BCAT1) (Luo et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

HGF/c‐MET pathway contributes to cisplatin‐mediated PD‐L1 expression in hepatocellular carcinoma

Zhang

Yang

Yao

et al. 2021

Cell Biology International

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Cisplatin has been reported to promote the expression of programmed cell death ligand-1 (PD-L1) in some cancer cells. However, the underlying mechanism through which PD-L1 is transcriptionally regulated by cisplatin in hepatocellular carcinoma (HCC) cells remains largely unknown. In the present study, we found that the expression of hepatocyte growth factor (HGF), p-Akt, p-ERK, and PD-L1 was increased in cisplatin-treated SNU-368 and SNU-739 cells. HGF stimulation also increased PD-L1 expression in these cells. Moreover, Inhibition of HGF/c-MET, PI3K/Akt, and MEK/ERK signaling pathways can dramatically block cisplatin or HGF-induced PD-L1 expression in SNU-368 and SNU-739 cells. In vivo, combination PHA665752 with cisplatin significantly reduced tumor weight with increased infiltration of CD8 + T cells in the tumor. Taken together, our study suggested that HGF/c-Met axis-induced the activation of PI3K/Akt and MEK/ERK pathways contributes to cisplatin-mediated PD-L1 expression. These findings may provide an alternative avenue for the treatment of HCC.

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“…The downstream of DEPDC1B, KIF23, is a member of kinesin motor protein involved in the regulation of cytokinesis and acts as an important regulator in cancer biology [ 33 ]. In this paper, similar to DEPDC1B, KIF23 expression was also upregulated in HCC cells.…”

Section: Discussionmentioning

confidence: 99%

“…Like DEPDC1B, KIF23 was overexpressed in various cancers, such as pancreatic cancer, breast cancer and primary lung cancer [ 34–36 ]. In addition, a study revealed that KIF23 expression was significantly upregulated in HCC cells, and the knockdown of KIF23 inhibited the proliferation of HCC cells by affecting the cell cycle [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

DEP domain containing 1B (DEPDC1B) exerts the tumor promoter in hepatocellular carcinoma through activating p53 signaling pathway via kinesin family member 23 (KIF23)

Shen¹,

Zhang

2022

Bioengineered

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Hepatocellular carcinoma (HCC) is closely associated with chronic liver disease and possesses a high incidence. DEP domain containing 1B (DEPDC1B) expression has been found to be upregulated in HCC according to bioinformatics analysis. This paper sought to study the specific role of DEPDC1B in HCC. The data of DEPDC1B expression and individual overall survival in HCC and normal liver tissues were acquired from UALCAN database. The association between DEPDC1B and the downstream signal, kinesin family member 23 (KIF23), was determined using LinkedOmics and STRING database, and subsequently confirmed by co-immunoprecipitation assay. The expression levels of DEPDC1B and KIF23 in normal hepatic epithelial cells and HCC cell lines were assessed by RT-qPCR and Western blotting, respectively. Following transfection with small interference RNA-DEPDC1B, the influences of DEPDC1B knockdown on cell proliferation, colony formation, cell cycle, cell invasion, migration, and KIF23 expression were evaluated. In addition, the effects of KIF23 overexpression on the above aspects of HCC cells were also determined, as well as the expression level of p53 signaling-related proteins. The results indicated that DEPDC1B was highly expressed in HCC cells. DEPDC1B knockdown inhibited the proliferation, migration, invasion, cycle, and KIF23 expression in HCC cells. Moreover, KIF23 overexpression reversed the inhibitory effect of DEPDC1B knockdown in HCC cells and the activation of the p53 signaling. In conclusion, DEPDC1B knockdown exerts anti-cancer role in HCC by activating the p53 signaling through KIF23.

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KIF14 and KIF23 Promote Cell Proliferation and Chemoresistance in HCC Cells, and Predict Worse Prognosis of Patients with HCC

Cited by 23 publications

References 52 publications

Tumor infiltrating lymphocytes associated competitive endogenous RNA networks as predictors of outcome in hepatic carcinoma based on WGCNA analysis

Tumor infiltrating lymphocytes associated competitive endogenous RNA networks as predictors of outcome in hepatic carcinoma based on WGCNA analysis

HGF/c‐MET pathway contributes to cisplatin‐mediated PD‐L1 expression in hepatocellular carcinoma

DEP domain containing 1B (DEPDC1B) exerts the tumor promoter in hepatocellular carcinoma through activating p53 signaling pathway via kinesin family member 23 (KIF23)

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