KIF18B promotes tumor progression through activating the Wnt/&amp;beta;-catenin pathway in cervical cancer

Wu, Yaqin; Wang, Anpeng; Zhu, Biqing; Huang, Jian; Lu, Emei; Xu, Hanzi; Xia, Wenjie; Dong, Gaochao; Jiang, Feng; Xu, Lin

doi:10.2147/ott.s157440

Cited by 51 publications

(75 citation statements)

References 38 publications

(35 reference statements)

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“…KIF18B, a member of the Kinesin‐8 family in humans, has been shown to express in a cell cycle‐dependent manner and supposed to take a critical role in cell division . The overexpression of KIF18B in hepatic carcinoma and cervical cancer has been reported recently, hinting that it is closely correlated with tumor progression. Our study first reported that KIF18B is highly expressed in cutaneous melanoma and is correlated with shorter overall survival time.…”

Section: Discussionsupporting

confidence: 92%

“…Previously, bioinformatic analyses by Itzel et al found that KIF18B is increased in breast, lung, liver, ovarian and renal cancer. In vitro and in vivo biological experiments showed that KIF18B functioned as a promoter in cervical cancer proliferation and metastasis . However, the detailed function of KIF18B in human tumors remains to be clarified.…”

Section: Introductionmentioning

confidence: 99%

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Kinesin family member 18B: A contributor and facilitator in the proliferation and metastasis of cutaneous melanoma

Yan

Zhu

Zhang

2019

J Biochem & Molecular Tox

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Melanoma is the most aggressive type of cutaneous tumor and the occurrence of metastasis makes it resistant to almost all available treatment and becomes incorrigible. Hence, identifying metastasis‐related biomarkers and effective therapeutic targets will assist in preventing metastasis and ameliorating cutaneous melanoma. In our present study, we reported kinesin family member 18B (KIF18B) as a novel contributor in cutaneous melanoma proliferation and metastasis, and it was found to be of great significance in predicting the prognosis of cutaneous melanoma patients. Bioinformatics analysis based on ONCOMINE, The Cancer Genome Atlas, and Genotype‐Tissue Expression database revealed that KIF18B was highly expressed in cutaneous melanoma and remarkably correlated with unfavorable clinical outcomes. Consistently, the results of the quantitative real‐time polymerase chain reaction exhibited that the expression of KIF18B was significantly higher in cutaneous melanoma cell lines than that in normal cells. In vitro, biological assays found that knockdown of KIF18B in cutaneous melanoma cells noticeably repressed cell proliferation, migration, and invasion, while inducing cell apoptosis. Moreover, the protein expression of E‐cadherin was enhanced while the expression of N‐cadherin, vimentin, and Snail was decreased in M14 cells after knocking down KIF18B. In addition, the phosphorylation of phosphoinositide 3‐kinase (PI3K) and extracellular‐signal‐regulated kinase (ERK) was significantly suppressed in M14 cells with silenced KIF18B. Above all, our results indicated that the repression of cutaneous melanoma cell migration and proliferation caused by KIF18B depletion suggested an oncogenic role of KIF18B in cutaneous melanoma, which acts through modulating epithelial‐mesenchymal transition and ERK/PI3K pathway.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Kinesin family member 18B: A contributor and facilitator in the proliferation and metastasis of cutaneous melanoma

Yan

Zhu

Zhang

2019

J Biochem & Molecular Tox

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“…In recent years, there are few studies on the effects of KIF18B on tumorigenesis. Previous study indicated that KIF18B promoted cancer development through the activation of Wnt/β‐catenin pathway in cervical cancer (Wu et al, ). Additionally, KIF18B was obviously associated with the poor prognosis of patients with hepatic carcinoma (Wu et al, ).…”

Section: Discussionmentioning

confidence: 95%

“…Previous study indicated that KIF18B promoted cancer development through the activation of Wnt/β‐catenin pathway in cervical cancer (Wu et al, ). Additionally, KIF18B was obviously associated with the poor prognosis of patients with hepatic carcinoma (Wu et al, ). Herein, we found a significant link between KIF18B expression and the poor prognosis of PDAC patients, and the different roles of KIF18B in these tumors were also worth further study.…”

Section: Discussionmentioning

confidence: 95%

“…KIF18B is highly expressed in cervical cancer tissue and further promotes the proliferation and migration of cervical cancer cells (Wu et al, ). Similarly, KIF18B is related to the poor prognosis of patients with hepatic carcinoma (Wu et al, ). KIF18B is widely expressed in various of tumor tissues, however, the potential link between KIF18B and PDAC is still unclear.…”

Section: Introductionmentioning

confidence: 99%

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KIF18B promotes the proliferation of pancreatic ductal adenocarcinoma via activating the expression of CDCA8

Liu

Zhang

et al. 2019

Journal Cellular Physiology

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Pancreatic cancer is one of the malignant tumors with the worst prognosis, and the 5-year survival rate of this disease is less than 1%. About 90% of pancreatic cancer is pancreatic ductal adenocarcinoma (PDAC), and targeting therapy has become a promising treatment for PDAC in recent years. To improve the survival rate, novel therapeutic targets for PDAC are still urgently needed. KIF18B was initially identified as a member of the kinesin family and involved in multiple cellular processes, such as separation of chromosomes in mitosis. Recently, it was found that KIF18B was involved in the growth and development of multiple cancers. However, the potential link between KIF18B and PDAC is still unclear. In this study, we demonstrated that KIF18B was highly expressed in human PDAC tissues, and related with the poor prognosis and clinical features, such as tumor size (*p = .013) and pTNM stage (*p = .025), of patients with PDAC. We further found that KIF18B knockdown blocked the cell proliferation of PDAC in vitro and in vivo, and the cell cycle was arrested caused by KIF18B depletion. Additionally, we also found that KIF18B bound to the promoter region of the cell division cycle associated 8 and thus activated its transcription. Taken together, this study explored the molecular mechanism underlying KIF18B promoting PDAC and provided a novel therapeutic target of this disease. K E Y W O R D SCDCA8, KIF18B, pancreatic ductal adenocarcinoma, proliferation, therapeutic target

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Silencing of KIF18B restricts proliferation and invasion and enhances the chemosensitivity of breast cancer via modulating Akt/GSK‐3β/β‐catenin pathway

Jiang

Liu

et al. 2021

BioFactors

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Kinesin family member 18B (KIF18B) is a new tumor-associated protein that contributes to the carcinogenesis of multiple malignancies. However, the detailed relevance of KIF18B in breast cancer has not been fully elucidated.This work aimed was to evaluate a possible relationship between KIF18B and breast cancer progression. Our findings show KIF18B is increased in breast cancer and demonstrate that high KIF18B level predicts a reduced survival rate. Cellular functional studies revealed that knockdown of KIF18B markedly reduces the proliferation, invasion, and epithelial-mesenchymal transition of breast cancer cells and enhances their chemosensitivity toward doxorubicin. Further studies showed that KIF18B modulates the level of phospho-Akt, phospho-glycogen synthase kinase-3β, and β-catenin. Notably, suppression of Akt abolished KIF18B-overexpression-induced increases in activation of Wnt/β-catenin pathway. In addition, re-expression of β-catenin reversed KIF18B-silencing-induced cancer-promoting effect. In vivo animal experiments elucidated that knockdown of KIF18B significantly weakened the tumorigenicity of breast cancer cells. Taken together, data of this study illustrate that KIF18B exerts a potential cancer-promoting function in breast cancer via enhancement of Wnt/β-catenin pathway through modulation of the Akt/GSK-3β axis.

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KIF18B promotes tumor progression through activating the Wnt/β-catenin pathway in cervical cancer

Cited by 51 publications

References 38 publications

Kinesin family member 18B: A contributor and facilitator in the proliferation and metastasis of cutaneous melanoma

Kinesin family member 18B: A contributor and facilitator in the proliferation and metastasis of cutaneous melanoma

KIF18B promotes the proliferation of pancreatic ductal adenocarcinoma via activating the expression of CDCA8

Silencing of KIF18B restricts proliferation and invasion and enhances the chemosensitivity of breast cancer via modulating Akt/GSK‐3β/β‐catenin pathway

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