KIF23 Promotes Gastric Cancer by Stimulating Cell Proliferation

Li, Xiaolong; Ji, Yaming; Song, Rui; Li, Xiaoning; Guo, Lan-Shuan

doi:10.1155/2019/9751923

Cited by 49 publications

(45 citation statements)

References 27 publications

(35 reference statements)

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“…Overexpression of KIF23 in non-small cell lung cancer (NSCLC) governs the crucial functions of KIF23 in regulating the cancerous properties of the cells [16]. KIF23 has been found to increase in GC and silencing KIF23 suppressed cell proliferation recently [5]. Consistently, the public datasets and our experimental results confirmed that KIF23 was upregulated in GC tissues and that expression of KIF23 was relatively high in advanced tumor tissues.…”

Section: Discussionsupporting

confidence: 84%

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KIF23 activated Wnt/β-catenin signaling pathway through direct interaction with Amer1 in gastric cancer

Liu

Chen

Dong

et al. 2020

Aging

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Increased expression of the kinesin family member 23 (KIF23) has been verified in gastric cancer (GC) and its upregulation contributes to cell proliferation. Even though, the role of KIF23 has not been fully elucidated in GC, and the mechanisms of KIF23 as an oncogene remain unknown. To further identify its potential role in GC, we analyzed gene expression data from GC patients in GEO and TCGA datasets. KIF23 was upregulated in GC, and increased expression of KIF23 correlated with poor prognosis. Importantly, KIF23 inhibition not only suppressed GC cell proliferation, tumorigenesis, but also migration and invasion, and arrested the cell cycle in the G2/M phase. Mechanistic investigations confirmed that KIF23 activated the Wnt/β-catenin signaling pathway by directly interacting with APC membrane recruitment 1 (Amer1). Furthermore, KIF23 exhibited competitive binding with Amer1 to block the association of Amer1 with adenomatous polyposis coli (APC), thus relocating Amer1 from the membrane and cytoplasm to the nucleus and attenuating the ability of Amer1 to negatively regulate Wnt/β-catenin signaling, resulting in activation of this signaling pathway. Collectively, our findings demonstrated that KIF23 promoted GC cell proliferation by directly interacting with Amer1 and activating the Wnt/β-catenin signaling pathway.

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Section: Discussionsupporting

confidence: 84%

“…Kato T et al verified that KIF23 was upregulated in lung cancer and predicted a poor clinical outcome [4]. Recently, Xiaolong Li found that KIF23 upregulated in GC and silencing KIF23 suppressed cell proliferation [5]. However, to date, the mechanisms of KIF23 in cancer remain unknown.…”

Section: Introductionmentioning

confidence: 99%

KIF23 activated Wnt/β-catenin signaling pathway through direct interaction with Amer1 in gastric cancer

Liu

Chen

Dong

et al. 2020

Aging

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“…Accordingly, KIF11 was supposed to be the novel therapeutic target of meningioma. Moreover, KIF23 was highly expressed in gastric cancer cells and it accelerated the progression of gastric cancer [17]. In our research, we investigated the function of KIF15 in breast cancer.…”

Section: Discussionmentioning

confidence: 95%

ZNF367-induced transcriptional activation of KIF15 accelerates the progression of breast cancer

Zeng¹,

Li²,

Zhai³

et al. 2020

Int. J. Biol. Sci.

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Breast cancer (BC) is one of the most common female cancers, and its incidence has been increasing in recent years. Although treatments are continuously improving, the prognosis of patients in the advanced stage is still unsatisfactory. Thus, an in-depth understanding of its molecular mechanisms is necessary for curing breast cancer. KIF15 is a tetrameric spindle motor which can regulate mitosis in cellular process and exert the crucial functions in several cancers. The purpose of our research was to investigate the functions of KIF15 in breast cancer. We tested the expression of KIF15 in breast cancer tissues and the survival rate of breast cancer patients with high or low level of KIF15 through TCGA data. What's more, western blot and immunohistochemistry assay were utilized to evaluate the protein level and mRNA level of KIF15 in breast cancer tissues. Then CCK-8, wound healing, transwell and flow cytometry experiments were adopted separately to test cell viability, migration, invasion and cell cycle distribution. We discovered that KIF15 was highly expressed in breast cancer tissues and high level KIF15 was associated with a low survival rate of breast cancer patients. Moreover, silence of KIF15 suppressed cell viability, migration, invasion and cell cycle distribution. Following, we discovered that ZNF367 was the upstream transcription factor of KIF15. In addition, silenced ZNF367 could also repress the growth of breast cancer cells. And rescue experiments indicated that overexpressed KIF15 could counteract the inhibition effect of silencing ZNF367 on the progression of breast cancer. Importantly, we discovered that KIF15 and ZNF367 were associated with the regulation of cell cycle. In short, ZNF367-activated KIF15 accelerated the progression of breast cancer by regulating cell cycle progress.

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“…Studies have shown that KIF23, as a member of the kinesin superfamily 6, is highly expressed in gastric cancer and is positively correlated with pTNM stage and poor prognosis. Knocking down KIF23 can inhibit the proliferation of gastric cancer cells [28]. Sun [29] [30].…”

Section: Discussionmentioning

confidence: 99%

Identification of KIF23 as a prognostic signature for ovarian cancer based on large scale samples and clinical validation

Zheng

Wang

et al. 2020

Preprint

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Background: Ovarian cancer is one of the common malignant tumors in gynecology. Although the treatment strategy for ovarian cancer has been greatly improved in recent years, due to the metastasis, recurrence and drug resistance, the 5-year overall survival rate of patients is still less than 47%. However, at present, there is no specific markers for clinical application. The purpose of this study is to verify the expression and clinical significance of KIF23 in ovarian cancer and identify potential targets for the clinical treatment of ovarian cancer. Methods: The expression of KIF23 in ovarian cancer tissues and its relationship between survival prognosis and clinical pathological parameters were analyzed in Oncomine, GEO, and TCGA databases. KIF23 expression was analyzed by Kaplan-Meier plotter database and its relationship with chemo-resistance was studied. The molecular mechanism involved in KIF23 was analyzed from the perspective of gene mutation, copy number variation and other genomics. Finally, immunohistochemistry experiment was used to verify the expression of KIF2, and its relationship between the clinical pathological parameters and prognosis of ovarian cancer patients was analyzed by single factor and multivariate Cox regression models. Results: Bioinformatic and experimental results have demonstrated that KIF23 is highly expressed in ovarian cancer, and its high expression is positively correlated with poor prognosis. Overexpression of KIF23 can cause chemotherapy resistance in ovarian cancer and affect the overall survival of patients. Genomics analysis showed that KIF23 expression was associated with mutations such as FLG2 and TTN, and it was significantly enriched in tumor signaling pathways such as DNA replication and cell cycle. Conclusions: KIF23 can not only be used as a biomarker of poor prognosis in patients with various stages of ovarian cancer, but also be used as a molecular targeted drug and an independent prognostic biomarker for the treatment of ovarian cancer patients.

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KIF23 Promotes Gastric Cancer by Stimulating Cell Proliferation

Cited by 49 publications

References 27 publications

KIF23 activated Wnt/β-catenin signaling pathway through direct interaction with Amer1 in gastric cancer

KIF23 activated Wnt/β-catenin signaling pathway through direct interaction with Amer1 in gastric cancer

ZNF367-induced transcriptional activation of KIF15 accelerates the progression of breast cancer

Identification of KIF23 as a prognostic signature for ovarian cancer based on large scale samples and clinical validation

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