KIAA0101 is a novel transcriptional target of FoxM1 and is involved in the regulation of hepatocellular carcinoma microvascular invasion by regulating epithelial-mesenchymal transition

Zhang, Tao; Guo, Jianxin; Gu, Jian; Chen, Ke; Wang, Zheng; Li, Huili; Wang, Guobin; Wang, Jiliang

doi:10.7150/jca.29490

Cited by 33 publications

(24 citation statements)

References 32 publications

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“…In the tumor setting of human gastric cancer, Zhu et al reported that increased KIAA0101 was a risk marker for recurrence [14]. As for the possible mechanism behind the pro-tumor effect, KIAA0101 was reported to be involved in tumor invasion and recurrence by promoting epithelial-to-mesenchymal transition (EMT) by Zhang et al and Jin et al [13,16]. Based on the prior literature, we speculate that KIAA0101 might partly involve in EMT in NSCLC.…”

Section: Discussionmentioning

confidence: 74%

Overexpression of KIAA0101 Promotes the Progression of Non-small Cell Lung Cancer

et al. 2020

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Lung cancer is the leading cause of cancer related death worldwide, with a continue-rising incidence. The proliferating cell nuclear antigen binding protein KIAA0101 is highly expressed in various types of cancer, including non-small cell lung cancer (NSCLC). However, its biological role and underlying mechanisms in NSCLC remains unclear. We downloaded KIAA0101 mRNA and clinical data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), and verified the KIAA0101 expression by conducting experiments of immunochemistry (IHC), immunofluorescence (IF), quantitative real-time PCR (qRT-PCR) and western-blot. Functional experiments were performed to explore the biological roles in vitro and in vivo. The results showed that KIAA0101 was overexpressed in NSCLC tissues and cell lines. High KIAA0101 expression was associated with high T stage, nodal invasion, advanced tumor stage, and poor overall survival (P<0.01). The receiver operating characteristic (ROC) curves showed that KIAA0101 could distinguish NSCLC from paired normal tissues with statistical significance (AUC=0.969, P<0.001). The multivariate analysis revealed that KIAA0101 was an independent prognostic factor for overall survival (HR=1.249, 95% CI: 1.001-1.559, P=0.049). Furthermore, KIAA0101 knockdown induced G1 phase cell cycle arrest and inhibited NSCLC cell proliferation and migration. We also found that the depletion of KIAA0101 decreased tumor volume in nude mice. In summary, our findings suggested that KIAA0101 was a reliable diagnostic and prognostic factor in NSCLC, with potential to be a promising treatment target.

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Section: Discussionmentioning

confidence: 74%

Overexpression of KIAA0101 Promotes the Progression of Non-small Cell Lung Cancer

et al. 2020

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“…Real-Time Polymerase Chain Reaction (qRT-PCR). Total RNA from tissue samples or cells was extracted by using TRIzol reagent according to the manufacturer's instructions as previously described [25]. For qPCR, reverse transcription was conducted with HiScript® II Q RT SuperMix (+gDNA wiper) according to the manufacturer's protocol.…”

Section: Rna Isolation Reverse Transcription and Quantitativementioning

confidence: 99%

Renalase Attenuates Mouse Fatty Liver Ischemia/Reperfusion Injury through Mitigating Oxidative Stress and Mitochondrial Damage via Activating SIRT1

Zhang

Guo

et al. 2019

Oxidative Medicine and Cellular Longevity

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Liver ischemia/reperfusion (IR) injury is a severe complication of liver surgery. Moreover, nonalcoholic fatty liver disease (NAFLD) patients are particularly vulnerable to IR injury, with higher rates of postoperative morbidity and mortality after liver surgeries. Our previous study found that renalase (RNLS) was highly sensitive and responsive to oxidative stress, which may be a promising biomarker for the evaluation of the severity of liver IR injury. However, the role of RNLS in liver IR injury remains unclear. In the present study, we intensively explored the role and mechanism of RNLS in fatty liver IR injury in vivo and in vitro. C57BL/6 mice were divided into 2 groups feeding with high-fat diet (HFD) and control diet (CD), respectively. After 20 weeks’ feeding, they were suffered from portal triad blockage and reflow to induce liver IR injury. Additionally, oleic acid (OA) and tert-butyl hydroperoxide (t-BHP) were used in vitro to induce steatotic hepatocytes and to simulate ROS burst and mimic cellular oxidative stress following portal triad blockage and reflow, respectively. Our data showed that RNLS was downregulated in fatty livers, and RNLS administration effectively attenuated IR injury by reducing ROS production and improving mitochondrial function through activating SIRT1. Additionally, the downregulation of RNLS in the fatty liver was mediated by a decrease of signal transduction and activator of transcription 3 (STAT3) expression under HFD conditions. These findings make RNLS a promising therapeutic strategy for the attenuation of liver IR injury.

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“…KIAA0101 (also referred to as NS5ATP9 or Paf15) is involved in multiple biological activities, including DNA repair, cell proliferation, cell cycle progression, and cell migration ( 5 ). Previous studies have shown that the KIAA0101 protein is dysregulated in a variety of malignant tumors and that its overexpression is associated with poor prognosis in patients with cancer ( 6 – 8 ). A recent study by our group showed that KIAA0101 protein expression was upregulated in ESCC tissues, and is associated with the pathological Tumor-Node-Metastasis (pTNM) stage, resistance to chemotherapy, tumor recurrence, and poor survival of patients with ESCC ( 7 ).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑216a‑5p suppresses esophageal squamous cell carcinoma progression by targeting KIAA0101

Sun

Yan

et al. 2020

Oncol Rep

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The KIAA0101 protein (also referred to as NS5ATP9 or Paf15) is overexpressed in esophageal squamous cell carcinoma (ESCC) and is associated with disease progression and poor patient survival, but how KIAA0101 expression is regulated remains unknown. The relationship between tumor miR-216a-5p expression and prognosis in patients with ESCC was revealed by survival analyses. Quantitative reverse-transcriptase PCR and western blot analysis were used to evaluate miR-216a-5p and KIAA0101 expression in human ESCC tissues and cell lines. The targeting of KIAA0101 by miR-216a-5p was verified by dual-luciferase reporter assays. The EC9706 and TE1 cell lines were transfected with miR-216a-5p mimics and inhibitor, or KIAA0101-specific shRNA and KIAA0101-expressing plasmids, in order to evaluate the effect of manipulating miR-216a-5p and KIAA0101 expression on ESCC cell proliferation, cell cycle progression, migration, and invasion. miR-216a-5p was lowly expressed and inversely correlated with KIAA0101 protein expression in ESCC tissues and cell lines. Lower miR-216a-5p expression was associated with worse prognosis in patients with ESCC. miR-216a-5p negatively regulated KIAA0101 expression by directly targeting the 3'-untranslated region of the KIAA0101 mRNA. Overexpression of miR-216a-5p suppressed the proliferation, migration, and invasion of the ESCC cell lines, whereas inhibition of miR-216a-5p had the opposite effects. Meanwhile, KIAA0101 promoted ESCC migration and invasion, and its overexpression abolished the antitumor effects of miR-216a-5p mimics. As a tumor suppressor, miR-216a-5p targets KIAA0101 to inhibit the proliferation, migration, and invasion of ESCC. Therefore, the miR-216a-5p/KIAA0101 axis may be a potential target for ESCC treatment.

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KIAA0101 is a novel transcriptional target of FoxM1 and is involved in the regulation of hepatocellular carcinoma microvascular invasion by regulating epithelial-mesenchymal transition

Cited by 33 publications

References 32 publications

Overexpression of KIAA0101 Promotes the Progression of Non-small Cell Lung Cancer

Overexpression of KIAA0101 Promotes the Progression of Non-small Cell Lung Cancer

Renalase Attenuates Mouse Fatty Liver Ischemia/Reperfusion Injury through Mitigating Oxidative Stress and Mitochondrial Damage via Activating SIRT1

MicroRNA‑216a‑5p suppresses esophageal squamous cell carcinoma progression by targeting KIAA0101

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