Upregulation of miR‐374a promotes tumor metastasis and progression by downregulating LACTB and predicts unfavorable prognosis in breast cancer

Zhang, Jun; He, Yuting; Yu, Yan; Chen, Xiaolong; Cui, Guangying; Wang, Weiwei; Zhang, Xiaojian; Luo, Yi; Li, Juan; Ren, Fang; Ren, Zhigang; Sun, Ranran

doi:10.1002/cam4.1576

Cited by 40 publications

(45 citation statements)

References 26 publications

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“…Luciferase activity analysis was performed using the Dual‐Luciferase Reporter Assay System (Promega, USA) as previously reported . Briefly, cells were co‐transfected with 200 ng plasmid containing wild‐type or mutated vectors, as well as 60 nmol/L let‐7a.…”

Section: Methodsmentioning

confidence: 99%

CBX2 is a functional target of miRNA let‐7a and acts as a tumor promoter in osteosarcoma

Han

Cao

et al. 2019

Cancer Medicine

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Osteosarcoma is the most common type of primary malignant tumor of skeletal with poor prognosis in children and adolescents. Accumulating evidence indicates that CBX2 is overexpressed in multiple human neoplasm and play a critical role in tumorigenesis and progression. However, its functional role and upstream regulation mechanism in osteosarcoma remain unknown. In the present study, tissue microarray (TMA) analysis was performed to determine the association between CBX2 expression and clinical prognosis of osteosarcoma patients by immunohistochemistry. We also investigated the functional role of CBX2 using small interfering RNA (siRNA) in vitro and in vivo. Additionally, we confirmed the direct binding between CBX2 and let‐7a via qPCR, western blot and luciferase reporter assay. We found that CBX2 is dramatically upregulated in osteosarcoma tissues and high CBX2 expression was correlated with metastasis, recurrence, and chemotherapy response, as well as unfavorable prognosis in patients with osteosarcoma. Similar results were observed in a sarcoma cohort from The Cancer Genome Atlas (TCGA) dataset. Further experiments revealed that CBX2 knockdown significantly impeded osteosarcoma cell proliferation and invasion ability in vitro, and suppressed the tumor growth in tumor xenografts model. Mechanistically, we confirmed that CBX2 is a functional target of miRNA let‐7a. Overexpression of let‐7a inhibits osteosarcoma cell proliferation, which was reversed by CBX2 overexpression. Taken together, our study demonstrates that let‐7a/CBX2 plays a crucial role in osteosarcoma progression. CBX2 could serve as a promising prognostic biomarker and potential therapeutic target for osteosarcoma patients.

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Section: Methodsmentioning

confidence: 99%

CBX2 is a functional target of miRNA let‐7a and acts as a tumor promoter in osteosarcoma

Han

Cao

et al. 2019

Cancer Medicine

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“…The TCGA cervical cancer cohort (hereafter referred to as TCGA-CESC cohort) dataset consisted of 304 cervical cancer patients. The expression of mRNAs was normalized to Log 2 counts and then analysed by BRB-array tools as described previously [18].…”

Section: Bioinformatics Analysismentioning

confidence: 99%

P4HA2 contributes to cervical cancer progression via inducing epithelial-mesenchymal transition

Cao¹,

Han²,

Li³

et al. 2020

J. Cancer

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Background: Cervical cancer is one of the most common gynaecological malignancies. Emerging studies have documented that prolyl-4-hydroxylase α subunit 2 (P4HA2) is involved in multiple processes of cancer progression. However, the functional roles of P4HA2 in cervical cancer progression remain to be elucidated. Methods: P4HA2 mRNA and protein levels were examined in cervical cancer tissues and cell line by qRT-PCR and western blot. The correlation of the P4HA2 expression levels and prognosis of cervical cancer patients were analysed in TCGA cervical cancer cohort and tissue microarray (TMA) cohort. P4HA2 was silenced to evaluate its function on cervical cancer progression both in vitro and in vivo. Bioinformatics analysis was performed to investigate the underlying regulation mechanism of cervical cancer by P4HA2. Results: We found that P4HA2 are markedly upregulated in cervical cancer tissues in comparison with adjacent non-neoplastic tissues. In addition, upregulation of P4HA2 was associated with shorter overall survival (OS) and relapse-free survival (RFS). Functionally, we demonstrated that P4HA2 knockdown attenuated cell proliferation, migration and invasion of cervical cancer cells. Furthermore, xenograft tumor mouse model experiment showed silencing P4HA2 significantly inhibited tumor growth in vivo. Mechanistically, bioinformatics analysis revealed that epithelial-mesenchymal transition (EMT) was involved in cervical cancer progression regulated by P4HA2 and we further confirmed knockdown P4HA2 suppressed the EMT process. Conclusion: our results suggest that P4HA2 functions as an oncogene in promoting cervical cancer cell proliferation, migration and invasion by inducing EMT, which might be a promising prognostic factor and therapeutic target for cervical cancer.

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“…The detailed information of the patients and specimens used in this study has been well described in our previous study 38,39 . Briefly, the Pan-cancer Tissue microarray (Pancancer TMA) containing 10 tumor types (each type of cancer containing 20 specimens and adjacent non-tumor tissues) were constructed with clinical specimens obtained between April 2009 and December 2012 from the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, China.…”

Section: Patients and Specimensmentioning

confidence: 99%

E2F1 mediated DDX11 transcriptional activation promotes hepatocellular carcinoma progression through PI3K/AKT/mTOR pathway

Zhao

et al. 2020

Cell Death Dis

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The DEAD/DEAH box helicase 11 (DDX11) plays vital roles in regulating the initiation of DNA replication. However, its precise function and regulation in hepatocellular carcinoma (HCC) have never been reported yet. In the current study, we found that DDX11 was overexpressed in HCC tissues. High DDX11 expression was positively correlated with large tumor size, tumor multiplicity, late tumor-node-metastasis (TNM) stage and poor prognosis. Additional, gain-offunction and loss-of-function experimental results revealed that DDX11 overexpression promoted HCC cell proliferation, migration, invasion and inhibited cell apoptosis in vitro. Overexpression of DDX11 also enhanced HCC tumorigenicity in vivo. Furthermore, DDX11 was transcriptionally regulated by transcription factor E2F1 in HCC, as demonstrated by chromatin immunoprecipitation (Ch-IP) and luciferase reporter assays. Mechanistically, E2F1/DDX11 axis promoted HCC cell proliferation, migration and invasion, at least in part, through activating PI3K/AKT/mTOR signaling pathway. Conclusively, our study demonstrates that E2F1-enhanced DDX11 expression promotes HCC progression through PI3K/AKT/mTOR pathway and DDX11 might be a potential therapeutic and prognostic target for HCC treatment.

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Upregulation of miR‐374a promotes tumor metastasis and progression by downregulating LACTB and predicts unfavorable prognosis in breast cancer

Cited by 40 publications

References 26 publications

CBX2 is a functional target of miRNA let‐7a and acts as a tumor promoter in osteosarcoma

CBX2 is a functional target of miRNA let‐7a and acts as a tumor promoter in osteosarcoma

P4HA2 contributes to cervical cancer progression via inducing epithelial-mesenchymal transition

E2F1 mediated DDX11 transcriptional activation promotes hepatocellular carcinoma progression through PI3K/AKT/mTOR pathway

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