KIF20A Predicts Poor Survival of Patients and Promotes Colorectal Cancer Tumor Progression through the JAK/STAT3 Signaling Pathway

Zhang, Qi; Di, Jun; Ji, Zhiyu; Mi, Aoning; Li, Quanying; Du, Xuehui; Wang, Anpeng; Wang, Anlian; Changjiang, Qin

doi:10.1155/2020/2032679

Cited by 22 publications

(21 citation statements)

References 43 publications

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“…In addition, KIF23 and KIF20A, as members of the kinesin-6 subfamily, have similar functions in maintaining normal cell division 31 . Our previous studies have shown that high expression of KIF20A can significantly promote the proliferation of colorectal cancer, and it is related to the poor prognosis of colorectal cancer patients 32 . Therefore, we speculate that KIF23 may play a similar role as KIF20A in colorectal cancer.…”

Section: Discussionmentioning

confidence: 98%

Aberrant KIF23 expression is associated with adverse clinical outcome and promotes cellular malignant behavior through the Wnt/β-catenin signaling pathway in Colorectal Cancer

et al. 2021

J. Cancer

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Purpose: The aim of the present study was to reveal the clinicopathological significance and prognostic role of kinesin family member 23 (KIF23) in colorectal cancer (CRC) and characterize its biological function and the underlying mechanisms. Methods: Bioinformatics analysis, immunohistochemistry, Western blot and qRT-PCR were utilized to investigate the expression of KIF23 in CRC tissues. The CCK-8 assay, wound healing assay and Matrigel assay were used to detect cell proliferation, migration and invasion in vitro . Western blot, immunofluorescence staining and cell function experiment were performed to explore the underlying mechanism. Results: The overexpression of KIF23 was associated with T stage, N stage, M stage and TNM stage, and CRC patients with high KIF23 expression had a worse prognosis. KIF23 knockdown inhibits CRC cells proliferation, migration and invasion in vitro . The mechanism study determined that KIF23 activates the Wnt/β-catenin signaling pathway by promoting the nuclear translocation of β-catenin to regulate the malignant behavior of CRC cells. Conclusion: These results suggest that KIF23 may act as a putative oncogene and a potential therapeutic target in CRC.

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Section: Discussionmentioning

confidence: 98%

Aberrant KIF23 expression is associated with adverse clinical outcome and promotes cellular malignant behavior through the Wnt/β-catenin signaling pathway in Colorectal Cancer

et al. 2021

J. Cancer

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“…For example, activation of the TGF-β/Smad2 signaling pathway mediated by HMMR contributes to the chemoresistance of gastric cancer ( 41 ). KIF20A maintains a set of malignant characteristics in colorectal cancer by activating the JAK/STAT3 pathway ( 42 , 43 ). However, little is known about GPR87, PGM2L1, and ANKZF1 in PCa.…”

Section: Discussionmentioning

confidence: 99%

A Novel Risk Factor Model Based on Glycolysis-Associated Genes for Predicting the Prognosis of Patients With Prostate Cancer

et al. 2021

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BackgroundProstate cancer (PCa) is one of the most prevalent cancers among males, and its mortality rate is increasing due to biochemical recurrence (BCR). Glycolysis has been proven to play an important regulatory role in tumorigenesis. Although several key regulators or predictors involved in PCa progression have been found, the relationship between glycolysis and PCa is unclear; we aimed to develop a novel glycolysis-associated multifactor prediction model for better predicting the prognosis of PCa.MethodsDifferential mRNA expression profiles derived from the Cancer Genome Atlas (TCGA) PCa cohort were generated through the “edgeR” package. Glycolysis-related genes were obtained from the GSEA database. Univariate Cox and LASSO regression analyses were used to identify genes significantly associated with disease-free survival. ROC curves were applied to evaluate the predictive value of the model. An external dataset derived from Gene Expression Omnibus (GEO) was used to verify the predictive ability. Glucose consumption and lactic production assays were used to assess changes in metabolic capacity, and Transwell assays were used to assess the invasion and migration of PC3 cells.ResultsFive glycolysis-related genes were applied to construct a risk score prediction model. Patients with PCa derived from TCGA and GEO (GSE70770) were divided into high-risk and low-risk groups according to the median. In the TCGA cohort, the high-risk group had a poorer prognosis than the low-risk group, and the results were further verified in the GSE70770 cohort. In vitro experiments demonstrated that knocking down HMMR, KIF20A, PGM2L1, and ANKZF1 separately led to less glucose consumption, less lactic production, and inhibition of cell migration and invasion, and the results were the opposite with GPR87 knockdown.ConclusionThe risk score based on five glycolysis-related genes may serve as an accurate prognostic marker for PCa patients with BCR.

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“…For instance, leptin stimulates prostate cancer cell proliferation and migration through STAT3 (Gorrab et al, 2020). In addition, KIF20A knockout reduces colorectal cancer cell proliferation and migration by inhibiting the JAK/STAT3 pathway (Zhang et al, 2020). On the other hand, some studies illustrated that the Hoveniae Semen Seu Fructus Ethanol extract exhibits anti-inflammatory activity via MAPK, AP-1, and STAT in lipopolysaccharide (LPS)-stimulated RAW 264.7 and mouse peritoneal macrophages (Jeong et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Falcarindiol Enhances Cisplatin Chemosensitivity of Hepatocellular Carcinoma via Down-Regulating the STAT3-Modulated PTTG1 Pathway

et al. 2021

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Hepatocellular carcinoma (HCC) is the most frequent primary liver malignancy globally and the third leading cause of cancer-related death. Chemotherapy is one of the main methods in treating HCC, while recent studies have found that the resistance of HCC to chemotherapeutic drugs reduces the efficacy of the chemotherapy. Falcarindiol (FAD) is a cytotoxic and anti-inflammatory polyacetylenic oxylipin found in food plants of the carrot family (Apiaceae), while its role in HCC remains to be explored. Here, HCC cells (Huh7 and LM3) were treated with FAD at different doses. Cell proliferation was tested by the cell counting kit-8 (CCK-8) method and colony formation assay, while the apoptosis was monitored by flow cytometry. The profiles of apoptosis-related proteins (Bax, bcl2, and Caspase-3), DNA repair proteins (Rad51, BRCA1, and MDC1), and the signal transducer and activator of transcription 3 (STAT3)/Pituitary Tumor Transforming Gene 1 (PTTG1) were verified by western blot (WB) or quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The interaction between STAT3 and PTTG1 was verified by immunoprecipitation (IP). In addition, a xenograft tumor model was constructed in mice to explore the anti-tumor effects of FAD in vivo, and immunohistochemistry (IHC) was performed to count the number of Ki67-stained cells. As a result, FAD inhibited HCC cell proliferation and DNA repair, facilitated their apoptosis, and also enhanced cisplatin (DDP) chemosensitivity. The Combination Index (CI) evaluation showed that FAD and DDP had synergistic effects in repressing HCC cell proliferation. Besides, FAD dampened the STAT3/PTTG1 pathway expression. Further studies revealed that inhibiting STAT3 enhanced the inhibitive effect of FAD on HCC cells, whereas overexpressing PTTG1 attenuated the anti-tumor effect of FAD. Overall, our study illustrated that FAD is a potential anticancer drug and strengthens the chemosensitivity of HCC cells to DDP by inhibiting the STAT3/PTTG1 pathway.

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KIF20A Predicts Poor Survival of Patients and Promotes Colorectal Cancer Tumor Progression through the JAK/STAT3 Signaling Pathway

Cited by 22 publications

References 43 publications

Aberrant KIF23 expression is associated with adverse clinical outcome and promotes cellular malignant behavior through the Wnt/β-catenin signaling pathway in Colorectal Cancer

Aberrant KIF23 expression is associated with adverse clinical outcome and promotes cellular malignant behavior through the Wnt/β-catenin signaling pathway in Colorectal Cancer

A Novel Risk Factor Model Based on Glycolysis-Associated Genes for Predicting the Prognosis of Patients With Prostate Cancer

Falcarindiol Enhances Cisplatin Chemosensitivity of Hepatocellular Carcinoma via Down-Regulating the STAT3-Modulated PTTG1 Pathway

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