KIF-2C expression is correlated with poor prognosis of operable esophageal squamous cell carcinoma male patients

Duan, Hao; Zhang, Xu; Wang, Fei Xiang; Cai, Mu Yan; Guo, Wei; Yang, Hong; Fu, Jianhua; Tan, Zhichao; Fu, Xiafei; Long, Qi; Wang, Xin Ye; Lin, Pei

doi:10.18632/oncotarget.11492

Cited by 25 publications

(24 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…KIFs participate in various physiological activities related to cellular motility. Substantial evidence verifies that KIFs participate in the malignant biological behavior of cancers . KIF2A and KIF2C are overexpressed in immortalized human bronchial epithelial cells, and subsequently promote EMT in cancer cells .…”

Section: Discussionmentioning

confidence: 98%

Macrophage ERα promoted invasion of endometrial cancer cell by mTOR/KIF5B‐mediated epithelial to mesenchymal transition

Jing

Peng

et al. 2019

Immunol Cell Biol

View full text Add to dashboard Cite

Tumor‐associated macrophages (TAMs) exert tumor‐promoting effects. There have been reports that estrogen receptors (ERs) are expressed on the infiltrating macrophages of endometriosis, ovarian cancer and lung cancer. However, the role of ERs in macrophages is not well characterized. In this study, we identified that ER alpha (ERα) expression on the macrophages of human endometrial cancer was positively correlated with cancer progression. Conditioned medium from selective ERα agonist‐treated M2 macrophages induced the epithelial to mesenchymal transition (EMT) in endometrial cancer cells. However, this effect can be inhibited by ERα antagonist. Here, we showed that macrophages ERα‐engaged abundantly produced chemokine (C‐C motif) ligand 18 (CCL18), and its expression promoted the invasion of endometrial cancer cells by activating the extracellular signal‐regulated kinase 1/2 pathway, whereas suppressing CCL18 abrogated these effects. Furthermore, we identified that CCL18 derived from TAMs upregulated KIF5B expression to promote EMT via activating the PI3K/AKT/mTOR signaling pathway in endometrial cancer. Overall, our findings show how ERα‐engaged infiltrating macrophages initiate chronic inflammation and promote the aggressive progression of endometrial cancer cells. ERα‐positive TAMs act as drivers of endometrial cancer, which may become a potential therapeutic target.

show abstract

Section: Discussionmentioning

confidence: 98%

Macrophage ERα promoted invasion of endometrial cancer cell by mTOR/KIF5B‐mediated epithelial to mesenchymal transition

Jing

Peng

et al. 2019

Immunol Cell Biol

View full text Add to dashboard Cite

show abstract

“…KIF2C is up‐regulated in glioma samples compared with normal brain tissues, and it is associated with histopathological grades . In esophageal squamous cell carcinoma, prognosis was worse for male patients with higher KIF2C expression compared with other patients at the same TNM stage …”

Section: Discussionmentioning

confidence: 99%

KIF2C exerts an oncogenic role in nonsmall cell lung cancer and is negatively regulated by miR‐325‐3p

Gan

Lin

et al. 2019

Cell Biochemistry & Function

View full text Add to dashboard Cite

Nonsmall cell lung cancer (NSCLC) is one of the leading causes of cancer‐related death worldwide. Kinesin family member 2C (KIF2C), a modulator in microtubule depolymerization, bipolar spindle formation, and chromosome segregation, has been reported to take roles in cancer biology, but its role in NSCLC remains unclear. This study was intended to investigate the expression and function of KIF2C in NSCLC. Our results demonstrated that KIF2C was up‐regulated in NSCLC tissues and cell lines. The high expression of KIF2C in NSCLC tissues was significantly correlated with higher T stage (0.0078), worse differentiation status (0.0049), and lymph node metastasis (P < .0001). We also proved that the high expression level of KIF2C predicted worse prognosis of the patients. After knockdown of KIF2C, the proliferation and metastasis of NSCLC cells were inhibited. Luciferase reporter assay suggested that KIF2C was a target gene of miR‐325‐3p, which was reported to be a tumour suppressor in NSCLC. In conclusion, this study proved an oncogenic role of KIF2C in NSCLC and partly clarified the mechanism of its high expression. Our findings provided a useful insight into the mechanism of NSCLC progression and offered clues to novel therapy strategies.

show abstract

“…Previous studies have revealed that many KIFs are involved in the carcinogenesis of multiple human cancers, including lung cancer [17][18][19][20][21][22]. For example, KIFC1 is upregulated in human breast cancer [19], whereas KIF2C is upregulated in esophageal squamous cell carcinoma and is associated with poor prognosis [22].…”

Section: Discussionmentioning

confidence: 99%

“…For example, KIFC1 is upregulated in human breast cancer [19], whereas KIF2C is upregulated in esophageal squamous cell carcinoma and is associated with poor prognosis [22]. KIF14 expression is significantly increased in cervical tumor tissues, and its expression is positively associated with a high tumor stage, lymph node metastasis, and chemoresistance [23].…”

Section: Discussionmentioning

confidence: 99%

Increased KIF15 Expression Predicts a Poor Prognosis in Patients with Lung Adenocarcinoma

Qiao

Chen

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Lung cancer is the leading cause of cancer-related deaths worldwide. The outcome of patients with non-small cell lung cancer remains poor; the 5-year survival rate for stage IV non-small cell lung cancer is only 1.0%. KIF15 is a tetrameric kinesin spindle motor that has been investigated for its regulation of mitosis. While the roles of kinesin motor proteins in the regulation of mitosis and their potentials as therapeutic targets in pancreatic cancer have been described previously, the role of KIF15 in lung cancer development remains unknown. Methods: Paired lung carcinoma specimens and matched adjacent normal tissues were used for protein analysis. Clinical data were obtained from medical records. We first examined KIF15 messenger RNA expression in The Cancer Genome Atlas database, and then determined KIF15 protein levels using immunohistochemistry and western blotting. Differences between the groups were analyzed using repeated measures analysis of variance. Overall survival was analyzed using the Kaplan–Meier method. Cell-cycle and proliferation assays were conducted using A549, NCI-H1299, and NCI-H226 cells. Results: KIF15 was significantly upregulated at both the messenger RNA and protein levels in human lung tumor tissues. In patients with lung adenocarcinoma, KIF15 expression was positively associated with disease stages; high KIF15 expression predicted a poor prognosis. KIF15 knockdown using short hairpin RNA in two human lung adenocarcinoma cell lines induced G1/S phase cell cycle arrest and inhibited cell growth, but there was no effect in human lung squamous cell carcinoma. Conclusion: Our findings show that KIF15 is involved in lung cancer carcinogenesis. KIF15 could therefore serve as a specific prognostic marker for patients with lung adenocarcinoma.

show abstract

KIF-2C expression is correlated with poor prognosis of operable esophageal squamous cell carcinoma male patients

Cited by 25 publications

References 39 publications

Macrophage ERα promoted invasion of endometrial cancer cell by mTOR/KIF5B‐mediated epithelial to mesenchymal transition

Macrophage ERα promoted invasion of endometrial cancer cell by mTOR/KIF5B‐mediated epithelial to mesenchymal transition

KIF2C exerts an oncogenic role in nonsmall cell lung cancer and is negatively regulated by miR‐325‐3p

Increased KIF15 Expression Predicts a Poor Prognosis in Patients with Lung Adenocarcinoma

Contact Info

Product

Resources

About