Suppression of <scp>KIF</scp>14 expression inhibits hepatocellular carcinoma progression and predicts favorable outcome

Yang, Tao; Zhang, Xianbo; Zheng, Zhihong

doi:10.1111/cas.12128

Cited by 32 publications

(35 citation statements)

References 23 publications

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“…Additionally, the change in the anchorage-independent phenotype in ovarian cancer cell lines in response to either KIF14 overexpression or knockdown was much more marked than changes in their proliferative rate [ 33 ], as was also observed in HeLa and a lung cancer cell line [ 44 ]. Additional proof was provided in HCC cell lines, where knockdown of KIF14 signifi cantly reduced xenograft formation in mice through apoptosis mediated by the PI3K pathway [ 45 ].…”

Section: The Role Of Kif14 In Cancer Cellsmentioning

confidence: 71%

“…A follow-up study of 24 samples confi rmed this fi nding [ 50 ]. Yang et al studied a cohort of 30 HCCs and found that KIF14 mRNA was overexpressed in most primary tumors (23/30), and correlated signifi cantly with increased gene-specifi c DNA copy number [ 45 ]. When assessed in a larger cohort of HCCs (102) with associated clinicopathological variables, KIF14 mRNA expression increased with stage and grade, and was associated with poor outcome (decreased disease-free survival), indicating that KIF14 is an important gene involved in HCC, and a potential prognostic and therapeutic target.…”

Section: Kif14 Expression As a Tumor Marker And Prognostic Indicator mentioning

confidence: 85%

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Kif14: A Clinically Relevant Kinesin and Potential Target for Cancer Therapy

Thériault

Corson

2015

Kinesins and Cancer

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Section: The Role Of Kif14 In Cancer Cellsmentioning

confidence: 71%

Section: Kif14 Expression As a Tumor Marker And Prognostic Indicator mentioning

confidence: 85%

Kif14: A Clinically Relevant Kinesin and Potential Target for Cancer Therapy

Thériault

Corson

2015

Kinesins and Cancer

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“…48 Increased KIF14 expression was detected in glioma, hepatocellular carcinoma, cervical, and breast cancers, and its expression was positively associated with staging. [8][9][10]13,49 High level of KIF14 was also significantly correlated with chemoresistance in cervical and breast cancers. 7,9 Importantly, overexpression of KIF14 was associated with adverse clinical outcome, tumor metastasis, and tumor recurrence.…”

Section: Discussionmentioning

confidence: 96%

“…7,9 Importantly, overexpression of KIF14 was associated with adverse clinical outcome, tumor metastasis, and tumor recurrence. 9,[49][50][51] Functional study indicated that siRNA-mediated knockdown of KIF14 attenuated cell proliferation, inhibited cell cycle progression, and induced apoptosis in glioma. 13 Similar finding was observed when cell proliferation and migration of liver cancer cells were suppressed upon KIF14 silencing by RNA interference technique.…”

Section: Discussionmentioning

confidence: 99%

The kinesin KIF14 is overexpressed in medulloblastoma and downregulation of KIF14 suppressed tumor proliferation and induced apoptosis

Xia

et al. 2017

Laboratory Investigation

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Medulloblastoma (MB) is the most common malignant brain tumor in childhood. At present, there is no well-established targeted drug for majority of patients. The kinesin family member 14 (KIF14) is a novel oncogene located on chromosome 1q and is dysregulated in multiple cancers. The objectives of this study were to evaluate KIF14 expression and chromosome 1q copy number in MB, and to delineate its biological functions in MB pathogenesis. By quantitative RT-PCR and immunohistochemistry, we found KIF14 was overexpressed in MB. Increased KIF14 expression at protein level was strongly associated with shorter progression-free survival (P=0.0063) and overall survival (P=0.0083). Fluorescence in situ hybridization (FISH) analysis confirmed genomic gain of chromosome 1q in 17/93 (18.3%) of MB. Combined genetic and immunohistochemical analyses revealed that 76.5% of MB with 1q gain showed consistent overexpression of KIF14, and a tight link between chromosome 1q gain and KIF14 overexpression (P=0.03). Transient, siRNAs-mediated downregulation of KIF14 suppressed cell proliferation and induced apoptosis in two MB cell lines. Stably KIF14 knockdown by shRNAs inhibited cell viability, colony formation, migration and invasion, and tumor sphere formation in MB cells. We conclude that KIF14 is dysregulated in MB and is an adverse prognostic factor for survival. Furthermore, KIF14 is part of MB biology and is a potential therapeutic target for MB.

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“…3e). Further, we saw upregulation of E2F1 64 and CCNB1 65 and downregulation of KIF14 66 and CCNE2 67 , all participating in cell cycle regulation ( Fig. 3f).…”

Section: Ethanol-induced Steatosis In the Liver-chipmentioning

confidence: 83%

Modeling alcoholic liver disease in a human Liver-Chip

Nawroth

et al. 2020

Preprint

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Fatty liver disease (FLD), is a major public health burden that affects up to 30% of people in Western countries and leads to progressive liver injury, comorbidities, and increased mortality. Key risk factors for developing FLD are obesity and alcohol consumption, both of which are growing in prevalence worldwide. There is an urgent need for human-relevant preclinical models to improve our understanding of FLD progression to steatohepatitis and for the development of sensitive noninvasive diagnostics and therapies. Alcohol-induced liver disease (ALD) represents an ideal case for modeling FDL as ethanol exposure is a comparatively simpler trigger for experimental induction of the pathology, as opposed to the complexity of modeling the diet- and life-style induced FLD. Further, despite their different root causes several common characteristics in disease progression and deterioration of liver function in the two disease entities, highlighting the potential of an ALD microphysiological model for broad application in translational research. Here, we leverage our recently reported human Liver-Chip for toxicity applications, to expand the capabilities of the platform for broad application in translational research. We report the first in vitro modeling of ALD that uses human relevant blood alcohol concentrations (BAC) and affords multimodal profiling of clinically relevant endpoints. Our ALD Liver-Chip recapitulates established FLD markers in response to ethanol in a concentration-dependent manner, including lipid accumulation and oxidative stress. Importantly, we show that the ALD Liver-Chip supports the study of secondary insults, as patients with advanced ALD often show high blood endotoxin levels due to alcohol-associated increased intestinal permeability and barrier dysfunction. Moreover, owing to new developments in the design, the ALD Liver-Chip enables the measurement of structural changes of the bile canaliculi (BC) network as a novel in vitro quantitative readout of alcoholic liver toxicity. In summary, we report the development of a human ALD Liver-Chip as a new platform for modeling the progression of alcohol-induced liver injury with direct translation to clinical research.

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Suppression of KIF14 expression inhibits hepatocellular carcinoma progression and predicts favorable outcome

Cited by 32 publications

References 23 publications

Kif14: A Clinically Relevant Kinesin and Potential Target for Cancer Therapy

Kif14: A Clinically Relevant Kinesin and Potential Target for Cancer Therapy

The kinesin KIF14 is overexpressed in medulloblastoma and downregulation of KIF14 suppressed tumor proliferation and induced apoptosis

Modeling alcoholic liver disease in a human Liver-Chip

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