Downregulation of PIM1 regulates glycolysis and suppresses tumor progression in gallbladder cancer

Xue, Chen; He, Yuting; Hu, Qiuyue; Yu, Yan; Chen, Xiaolong; Chen, Jianan; Ren, Fang; Li, Juan; Ren, Zhigang; Cui, Guangying; Sun, Ranran

doi:10.2147/cmar.s184381

Cited by 19 publications

(18 citation statements)

References 31 publications

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“…PIM1 is significantly overexpressed in gallbladder cancer (GBC) tissue, and its expression level is positively correlated with clinical malignancies and poor prognosis. PIM1 is a promising therapeutic target for the treatment of human GBC [ 31 ]. In triple-negative breast cancer (TNBCs) tumors and their cell models, PIM1 expression is related to several transcription signals involving the transcription factor MYC.…”

Section: Discussionmentioning

confidence: 99%

Circular RNA CircITGA7 Promotes Tumorigenesis of Osteosarcoma via miR-370/PIM1 Axis

Fang

Wang

Guo

et al. 2020

Computational and Mathematical Methods in Medicine

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Many studies have shown that there are many circular RNA (circRNA) expression abnormalities in osteosarcoma (OS), and this abnormality is related to the development of osteosarcoma. But at present, it is unclear as to what circITGA7 has in the OS and what it does. In this study, qRT-PCR was used to detect the expression of circITGA7, miR-370, and PIM1 mRNA in OS tissues and cells. The CCK-8 assay was used to detect the effect of circITGA7 on cell proliferation. Later, the transwell assay was used to detect cell migration and invasion. The dual-luciferase reporter assay confirmed the existence of the targeting relationship between circITGA7 and miR-370, and miR-370 and PIM1. We found that circITGA7 was upregulated in OS tissues and cell lines. Knockdown of circITGA7 weakened the cell’s ability to proliferate and metastasize. Furthermore, we observed that miR-370 was negatively regulated by circITGA7, while PIM1 was positively regulated by it. A functional assay validated that circITGA7 promoted OS progression via suppressing miR-370 and miR-370 affected OS proliferation and migration via PIM6 in OS. In summary, this study shows that circITGA7 promotes OS proliferation and metastasis via miR-370/PIM1.

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Section: Discussionmentioning

confidence: 99%

Circular RNA CircITGA7 Promotes Tumorigenesis of Osteosarcoma via miR-370/PIM1 Axis

Fang

Wang

Guo

et al. 2020

Computational and Mathematical Methods in Medicine

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“…IHC was performed as previously reported 19, 20. Briefly, 5 μm thick TMA sections were deparaffinized and then treated with hydrogen peroxide to quench endogenous peroxidase activity.…”

Section: Methodsmentioning

confidence: 99%

The Role of Upregulated DDX11 as A Potential Prognostic and Diagnostic Biomarker in Lung Adenocarcinoma

Liu

et al. 2019

J. Cancer

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Background: Lung adenocarcinoma (ADC) is the main cause of cancer-related mortality in lung cancer patients. DEAD/DEAH box helicase 11 (DDX11) was previously shown to be dysregulated and to exert oncogenic activity in cancer. However, the diagnostic value and clinical significance of DDX11 in ADC remain unknown. Methods: A total of 513 ADC and 59 normal tissue samples were obtained from The Cancer Genome Atlas (TCGA) database, and the mRNA expression level of DDX11 in ADC was evaluated. Additionally, a meta-analysis of 7 ADC cohorts from the Gene Expression Omnibus (GEO) database was conducted to validate the DDX11 expression pattern. Moreover, receiver operating characteristic (ROC) curve analysis was used to identify the diagnostic power of DDX11 in ADC. A tissue microarray (TMA) comprising 86 ADC specimens and their adjacent normal specimens was applied to indicate DDX11 protein expression status. In addition, Kaplan-Meier and Cox regression analyses were conducted to validate the prognostic value of DDX11 in ADC. Finally, the molecular mechanism of DDX11 action in ADC was predicted by gene set enrichment analysis (GSEA). Results: DDX11 was upregulated in ADC tissues and was associated with worse overall survival (OS). ROC curves of DDX11 showed high values for diagnosis. Additionally, DDX11 expression has remarkable correlations with DNA replication and the cell cycle G1-S phase pathway. Consistently, it was associated with cell cycle genes, such as CCNA2, CCNB1, CCNC, CCND1, CCNE1, CDK2, CDK4 and CDK6. Moreover, high CCNA2, CCNB1, CCNE1 and CDK6 expression in ADC patients predicted worse OS and progression-free survival (PFS). Conclusion: DDX11 was significantly upregulated and predicted poor prognosis in ADC. This gene might serve as a potential novel prognostic and diagnostic biomarker for ADC.

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“…The Western blot was processed as previously described 12. The primary antibodies used in the present study were listed below: wnt3a (1:1000, ab19925, Abcam), β-catenin (1:1000, 51067-2-AP, Proteintech), Vimentin (1:1000, 10366-1-AP, Proteintech), E-cadherin (1:500, 20874-1-AP, Proteintech), N-cadherin (1:500, 22018-1-AP, Proteintech), Fibronectin (1:500, 15613-1-AP, Proteintech), Snail (1:500, 13099-1-AP, Proteintech) and GAPDH (1:2000, 60004-1-Ig, Proteintech).…”

Section: Methodsmentioning

confidence: 99%

“…These assays were performed as described previously and were detailed in the Supplementary Materials and Methods section 12,13…”

Section: Methodsmentioning

confidence: 99%

<p>CLK3 Is A Direct Target Of miR-144 And Contributes To Aggressive Progression In Hepatocellular Carcinoma</p>

Li¹,

Cui²,

Hu³

et al. 2019

OTT

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Background: Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer with high incidence. The underlying molecular mechanisms of HCC development have been intensively studied. CLK3 (CDC Like Kinase 3) is a nuclear dual-specificity kinase and regulates gene splicing. We investigated the expression profile and functional role of CLK3 in HCC. Methods: Immunohistochemistry (IHC) and Western blot were performed to determine CLK3 expression in HCC tissues. Bioinformatics analysis using TCGA and GEO database was conducted to evaluate the relationship between CLK3 expression and HCC prognosis. Cell proliferation was assessed by CCK8, EdU and colony formation assays, while transwell and wound-healing assays were performed to investigate the cell migration and invasion in vitro. Xenograft nude mouse model was used to test the function of CLK3 on tumor growth in vivo. Luciferase reporter assay, Western blot and RT-qPCR were conducted to verify the miRNA that directly targeted CLK3. Results: CLK3 was markedly upregulated in HCC tissues, and the expression levels of CLK3 were closely associated with TNM stages and HCC prognosis. Functional analysis indicated that knockdown of CLK3 could suppress HCC cell growth, invasion and migration in vitro, and inhibit tumor development in vivo. Moreover, CLK3 was demonstrated as a direct target of miR-144 and miR-144 expression was inversely correlated with CLK3 expression in HCC. Enforced overexpression of miR-144 markedly inhibited the CLK3 expression while overexpression of CLK3 partially reversed the inhibitory function of miR-144 on HCC cell growth and metastasis. Mechanistically, we found that miR-144 overexpression inhibited Wnt/β-catenin signaling and the inhibition could be partly abolished by overexpression of CLK3. Conclusion: In summary, we demonstrate tumor suppressor miR-144 suppresses hepatocellular carcinoma development and metastasis via regulating CLK3 and Wnt/β-catenin signaling, indicating that miR-144/CLK3 could be used for HCC diagnosis and treatment.

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Downregulation of PIM1 regulates glycolysis and suppresses tumor progression in gallbladder cancer

Cited by 19 publications

References 31 publications

Circular RNA CircITGA7 Promotes Tumorigenesis of Osteosarcoma via miR-370/PIM1 Axis

Circular RNA CircITGA7 Promotes Tumorigenesis of Osteosarcoma via miR-370/PIM1 Axis

The Role of Upregulated DDX11 as A Potential Prognostic and Diagnostic Biomarker in Lung Adenocarcinoma

<p>CLK3 Is A Direct Target Of miR-144 And Contributes To Aggressive Progression In Hepatocellular Carcinoma</p>

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