The downregulation of miR-3173 in B-cell acute lymphoblastic leukaemia promotes cell invasion via PTK2

Tian, Lijun; Cao, Junhua; Ji, Qiang; Zhang, Chuanling; Qian, Tong; Song, Xianchuan; Huang, Baoshan; Tian, Xinyi

doi:10.1016/j.bbrc.2017.10.013

Cited by 16 publications

(10 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Focal adhesion kinase (FAK) is one of the key components of the focal adhesion complex, which is a multi-protein structure that connects the extracellular matrix to the cytoskeleton of the cytoplasm, thus controlling cell adhesion, migration and invasion 13. Currently, overexpression of FAK is reported to be correlated with tumor invasiveness in several tumors, including hepatocellular carcinoma,14 colorectal cancer,15 leukemia,16 breast cancer,17 and lung adenocarcinoma18, etc. However, evidence of FAK implication in the EMT and metastasis of ESCC is limited.…”

Section: Introductionmentioning

confidence: 99%

<p>Downregulation of microRNA-4324 promotes the EMT of esophageal squamous-cell carcinoma cells via upregulating FAK</p>

Zhou¹,

Zhu²,

Jiang³

et al. 2019

OTT

View full text Add to dashboard Cite

Background: Esophageal squamous-cell carcinoma (ESCC) metastasis is the major cause of death of this severe and common malignancy. Focal adhesion kinase (FAK) is one of the key components of the focal adhesion complex, which is a multi-protein structure that controls cell adhesion, migration and invasion and regulates tumor metastasis. Purpose: To identify the roles and mechanisms of FAK in the regulation of Epithelial-to-mesenchymal transition (EMT) of ESCC cells. Methods: The expression of FAK and miR-4324 in both ESCC tissues and cells were evaluated by qRT-PCR and Immunohistochemistry analysis. Dual luciferase assays were performed for the confirmation of miR-4324’s specific binding to 3’UTR of FAK mRNA. Besides, the trans-well assays and wound healing assays were employed to evaluate the effects of FAK /miR-4324 axis on the EMT regulation of ESCC cells. Furthermore, the relationship between miR-4374/FAK expression and clinical pathologic parameters & patient survival were also statistically analyzed. Results: In this study, we identified the upregulation of FAK and downregulation of miR-4324 in both ESCC cells and tissues. Overexpression of miR-4324 mimic, which significantly decreased cellular FAK levels, can impair the invasion potential and migration ability of ESCC cells. Besides, co-transfection of FAK can attenuate the function of miR-4324 mimic. Further experimental results demonstrated that miR-4324 mimic remarkably downregulated epithelial-to-mesenchymal transition (EMT) phenotype, which can also be effectively prevented by overexpressing FAK in ESCC cells. What’s more, low miR-4324 and high FAK tissue levels have significant association with poor cell differentiation, tumor size and invasion depth as well as overall number of metastatic lymph nodes. Patients with high miR-4324 and low FAK levels in tumoral tissues lived longer than their counterparts, respectively. Conclusions: In conclusion, miR-4324/FAK axis could be a promising therapeutic target and potential prognostic biomarker for ESCC, which deserves further investigation in the clinic.

show abstract

Section: Introductionmentioning

confidence: 99%

<p>Downregulation of microRNA-4324 promotes the EMT of esophageal squamous-cell carcinoma cells via upregulating FAK</p>

Zhou¹,

Zhu²,

Jiang³

et al. 2019

OTT

View full text Add to dashboard Cite

show abstract

“…The dysregulation of miR-3173 is implicated in the progression of ovarian carcinoma [ 49 ] and B-cell acute lymphoblastic leukemia [ 50 ]. In B-cell acute lymphoblastic leukemia, the downregulation of miR-3173 promotes cell invasion and tumorigenesis.…”

Section: Discussionmentioning

confidence: 99%

LINC00893 inhibits the progression of prostate cancer through miR-3173-5p/SOCS3/JAK2/STAT3 pathway

Fan

Liu

et al. 2022

Cancer Cell Int

View full text Add to dashboard Cite

Background Prostate cancer (PCa) is one of the most common malignant tumors in the male urinary system. In recent years, the morbidity and mortality of PCa have been increasing due to the limited effects of existing treatment strategies. Long non-coding RNA (lncRNA) LINC00893 was reported to inhibit the proliferation and metastasis of papillary thyroid cancer cells, but its role in PCa has not been reported. This study aims to investigate the role and underlying mechanism of LINC00893 in regulating the progression of PCa cells. Methods We first compared LINC00893 expression levels between PCa tissues and normal prostate tissues through TCGA database. The relative LINC00893 expression levels were further validated in 66 pairs of PCa tissues and para-cancerous normal tissues, as well as in PCa cell lines. Gain-of-function experiment was performed by transfecting PCa cell with LINC00893 expression vector, and CCK (Cell count kit)-8, 5-Ethynyl-2′-deoxyuridine (EdU) incorporation, colony information and transwell assays were conducted to assess the functional phenotypes. Dual-luciferase reporter, RNA-binding protein immunoprecipitation (RIP) and RNA pull-down assays were performed to evaluate the molecular interactions. Results LINC00893 was downregulated in PCa tissues and cell lines, and patients with low expression of LINC00893 were associated with a poorer overall survival rate. LINC00893 overexpression hindered the proliferation, epithelial-mesenchymal transition (EMT) as well as the migratory ability of PCa cells, and suppressed the tumorigenesis of PCa cells in nude mice. We further demonstrated that LINC00893 acted as a sponge for miR-3173-5p and inhibited its activity, which in turn regulated the suppressor of cytokine signaling 3 (SOCS3)/Janus Kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling axis. Conclusions Our study demonstrated that LINC00893 suppresses the progression of PCa cells through targeting miR-3173-5p/SOCS3/JAK2/STAT3 axis. Our data uncovers a novel tumor-suppressor role of LINC00893 in PCa, which may serve as a potential strategy for targeted therapy in PCa. Grapical Abstract

show abstract

“…At present, the research on miR-3173 in cancer is rarely involved. The only studies showed that miR-3173 is implicated in the progression of ovarian carcinoma [49] and B-cell acute lymphoblastic leukemia [50]. However, whether mir-3173 is involved in the development of PCA remains to be further studied.…”

Section: Discussionmentioning

confidence: 99%

LINC00893 Inhibits The Progression of Prostate Cancer Through miR-3173-5p/SOCS3/JAK2/STAT3 Pathway

Yu¹,

Fan²,

Liu³

et al. 2021

Preprint

View full text Add to dashboard Cite

Background: Prostate cancer (PCa) is one of the most common malignant tumors in the male urinary system. In recent years, the morbidity and mortality of PCa have been increasing due to the limited effects of existing treatment strategies. Long non-coding RNA (lncRNA) LINC00893 inhibits the proliferation and metastasis of papillary thyroid cancer (PTC) cells, but its role in PCa has not been reported. Our study aims to clarify the role and underlying mechanism of LINC00893 in regulating the progression of PCa.Methods: We analyzed LINC00893 expression through TCGA database. We also collected 66 paires of PCa tissues and matched para-cancerous tissues as well as cell lines and assessed LINC00893 expression. Subsequently, we conducted gain-of-function assays to confirm the role of LINC00893 in PCa. CCK-8, EdU, colony information and transwell assays were implemented to detect cell proliferation, colony formation and metastasis abilities, respectively. RT-qPCR and western blot assays were used to quantify the expression of mRNA and protein. Dual-luciferase reporter, RNA-binding protein immunoprecipitation (RIP) and RNA pull down assays were conducted to evaluate the interaction of molecules. Spearman correlation coefficient analysis was conducted to detect the correlation between molecules.Results: We found that the LINC00893 expression in PCa tissues and cell lines was upregulated compared with matched controls, and patients with low expression of LINC00893 suffered a low overall survival rate. Overexpression of LINC00893 hindered the proliferation, epithelial-mesenchymal transition (EMT) as well as metastasis of PCa cells in vitro and in vivo. In terms of mechanism, suppressor of cytokine signaling 3 (SOCS3)/Janus Kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway occupied a central position in the regulation of PCa progression by LINC00893. LINC00893 weakened the inhibition role of miR-3173-5p on SOCS3 expression through functioning as a miR-3173-5p sponge, which inhibited the JAK2/STAT3 signaling pathway. Conclusions: LINC00893 suppresses the progression of prostate cancer through miR-3173-5p/SOCS3/JAK2/STAT3 pathway. our data uncovers a novel mechanism by which LINC00893 hinders the progression of PCa, which enriches the molecular network of LINC00893 regulating the PCa progression and laies a theoretical foundation for PCa targeted therapy.

show abstract

The downregulation of miR-3173 in B-cell acute lymphoblastic leukaemia promotes cell invasion via PTK2

Cited by 16 publications

References 18 publications

<p>Downregulation of microRNA-4324 promotes the EMT of esophageal squamous-cell carcinoma cells via upregulating FAK</p>

<p>Downregulation of microRNA-4324 promotes the EMT of esophageal squamous-cell carcinoma cells via upregulating FAK</p>

LINC00893 inhibits the progression of prostate cancer through miR-3173-5p/SOCS3/JAK2/STAT3 pathway

LINC00893 Inhibits The Progression of Prostate Cancer Through miR-3173-5p/SOCS3/JAK2/STAT3 Pathway

Contact Info

Product

Resources

About