TGF-β1-Induced Upregulation of MALAT1 Promotes Kazakh's Esophageal Squamous Cell Carcinoma Invasion by EMT

Liu, Qing; Chen, Yumei; Liu, Tao; Han, Xiaodong; Zhang, Xiao; Shen, Tongxue; Lü, Xiaomei

doi:10.7150/jca.48426

Cited by 10 publications

(8 citation statements)

References 41 publications

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“…Recent studies have revealed that EMT exerts crucial roles in the invasion as well as metastasis of ESCC 30 . Nevertheless, the underlying mechanisms associated with EMT remain confusing.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have revealed that EMT exerts crucial roles in the invasion as well as metastasis of ESCC. 30 Nevertheless, the underlying mechanisms associated with EMT remain confusing. This investigation verified that the supression of EPPK1 significantly inhibits EMT progression, which indicates that EPPK1 might influence cell migration and invasion by mediating EMT.…”

Section: Discussionmentioning

confidence: 99%

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Epiplakin1 promotes the progression of esophageal squamous cell carcinoma by activating the PI3K‐AKT signaling pathway

et al. 2022

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Background Epiplakin1 (EPPK1) has been associated with disease progression and unfavorable prognosis of many cancers, but its functional involvement in esophageal squamous cell carcinoma (ESCC) remains to be uncovered. Methods The Quantitative Real‐time PCR (qPCR) assay was employed to determine the expression of EPPK1 in ESCC tissues and cells. CCK‐8 assay, colony forming assay, wound healing assay, and transwell invasion assay were utilized to evaluate the effects of EPPK1 on cell proliferation, migration, and invasion capacity in ESCC cells using small interfering ribonucleic acids. Flow cytometry was performed to estimate the cell apoptotic rate caused by silencing of EPPK1. The proteins related to epithelial‐to‐mesenchymal transition (EMT), apoptosis, and activation of the phosphatidylinositol 3‐kinase/serine threonine protein kinase 1 (PI3K/AKT) signaling pathway were measured by western blot. Results The expression of EPPK1 was dramatically increased in ESCC tissues and cells compared to that in relative controls. Additionally, silencing of EPPK1 suppressed ESCC cell growth, colony formation, migration, invasion, and EMT, while promoting ESCC cell apoptosis. Furthermore, EPPK1 induced ESCC cell progression via mediating the PI3K/AKT signaling pathway. Conclusion EPPK1 promotes ESCC progression by modulating the PI3K/AKT signaling pathway and could serve as a potential target for ESCC treatment.

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“…Recent studies have revealed that EMT exerts crucial roles in the invasion as well as metastasis of ESCC 30 . Nevertheless, the underlying mechanisms associated with EMT remain confusing.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Epiplakin1 promotes the progression of esophageal squamous cell carcinoma by activating the PI3K‐AKT signaling pathway

et al. 2022

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“…In the tongue squamous cell carcinoma, MALAT1 could promote EMT while inhibit the apoptosis by regulating the activity of Wnt/β‐catenin pathway 33 . Of note, MALAT1 knockdown inhibited the EMT in TGF‐β1‐induced esophageal squamous cell carcinoma 34 . Consistently, the down‐regulation of MALAT1 could block the EMT of EC cells, with down‐regulations of Vimentin and SNAIL and the up‐regulation of E‐cadherin, indicating that the down‐regulation of MALAT1 could be a therapeutic target to inhibit the metastasis and invasion of EC.…”

Section: Discussionmentioning

confidence: 96%

Dexmedetomidine inhibits the growth and metastasis of esophageal cancer cells by down‐regulation of lncRNA MALAT1

Zhang

Cai

et al. 2022

The Kaohsiung J of Med Scie

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This study aims to evaluate the effect of dexmedetomidine (DEX)—on esophageal cancer (EC) via regulating long noncoding RNA (lncRNA) metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1). The effect of DEX on MALAT1 expression and EC cell viability was detected. EC cells were divided into Blank, DEX, scrambled/MALAT1 siRNA, and DEX + control/MALAT1 groups, followed by a series of experiments including quantitative reverse‐transcription polymerase chain reaction (qRT‐PCR), western blotting, 3‐[4,5‐dimethylthiazol‐2‐yl]‐2,5 diphenyl tetrazolium bromide (MTT), Annexin V‐FITC/PI staining, wound healing, and Transwell assays. Additionally, mice were subjected to the subcutaneous injection of Eca109 cells transfected by control/MALAT1 activation lentiviral vector to construct EC models with the DEX treatment, and then the tumor volume and the expression of Ki‐67 and active caspase‐3 were determined. DEX reduced the expression of MALAT1 in EC cells in a dose‐dependent manner. DEX inhibited the viability of EC cells, but increased the cell apoptosis, which, however, was reversed by MALAT1 overexpression. Moreover, MALAT1 overexpression abolished the inhibitory effect of DEX on the epithelial–mesenchymal transition (EMT) of EC cells, with enhanced migration and invasion. Furthermore, DEX succeeded in decreasing the tumor volume with the down‐regulation of MALAT1. In comparison with the DEX group, mice in the DEX + MALAT1 group had larger tumors, with the up‐regulation of Ki‐67 and the down‐regulation of active caspase‐3. DEX can reduce the expression of MALAT1 in EC cells, thereby inhibiting the proliferation, invasion and migration, as well as EMT, and promoting the apoptosis of EC cells.

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“…This provides an evidence for a positive correlation between MALAT1 and EMT induction in CTCL cells because upregulation of epithelial marker with simultaneous downregulation of mesenchymal marker is reliable indication of reversal of EMT. The EMT induced by lncRNAs plays an important role in cancer metastasis ( 19 ) and accordingly MALAT1-induced EMT has been reported to regulate cancer metastasis ( 13 , 20 , 21 ). Thus, MALAT1 upregulation in CTCL can be related to a more aggressive disease.…”

Section: Discussionmentioning

confidence: 99%

Epigenetic regulation of cutaneous T-cell lymphoma is mediated by dysregulated lncRNA MALAT1 through modulation of tumor microenvironment

Guo

Guan²,

Chen³

et al. 2022

Front. Oncol.

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Cutaneous T-Cell Lymphoma (CTCL) is a rare non-Hodgkin lymphoma marked by migration of T-lymphocytes to the skin. It has many subtypes some of which are aggressive with documented metastasis. We investigated a possible role of lncRNA MALAT1 in CTCL cells because of its documented involvement in cancer metastasis. A screening of MALAT1 in CTCL patients revealed its elevated levels in the patients, compared to healthy individuals. For our investigation, we employed HH and H9 CTCL cells and silenced MALAT1 to understand the MALAT1 mediated functions. Such silencing of MALAT1 resulted in reversal of EMT and inhibition of cancer stem cell phenotype, along with reduced cell growth and proliferation. EMT reversal was established through increased E-cadherin and reduced N-cadherin while inhibition of cancer stem cell phenotype was evident through reduced Sox2 and Nanog. CTCL patients had higher circulating levels of IL-6, IL-8, IL-10, TGFβ, PGE2 and MMP7 which are factors released by tumor-associated macrophages in tumor microenvironment. MALAT1 sponged miR-124 as this tumor suppressive miRNA was de-repressed upon MALAT1 silencing. Moreover, downregulation of miR-124 attenuated MALAT1 silencing effects. Our study provides a rationale for further studies focused on an evaluation of MALAT1-miR-124 in CTCL progression.

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TGF-β1-Induced Upregulation of MALAT1 Promotes Kazakh's Esophageal Squamous Cell Carcinoma Invasion by EMT

Cited by 10 publications

References 41 publications

Epiplakin1 promotes the progression of esophageal squamous cell carcinoma by activating the PI3K‐AKT signaling pathway

Epiplakin1 promotes the progression of esophageal squamous cell carcinoma by activating the PI3K‐AKT signaling pathway

Dexmedetomidine inhibits the growth and metastasis of esophageal cancer cells by down‐regulation of lncRNA MALAT1

Epigenetic regulation of cutaneous T-cell lymphoma is mediated by dysregulated lncRNA MALAT1 through modulation of tumor microenvironment

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