TGF-β regulates the ERK/MAPK pathway independent of the SMAD pathway by repressing miRNA-124 to increase MALAT1 expression in nasopharyngeal carcinoma

Du, Mengnan; Chen, Wei; Zhang, Wenjun; Tian, Xiaokang; Wang, Tingting; Wu, Jing; Gu, Jian; Zhang, Nan; Lü, Zhiwei; Qian, Lu‐Xi; Qian, Fei; Wang, Yan; Peng, Fanyu; He, Xia; Li, Yin

doi:10.1016/j.biopha.2018.01.120

Cited by 29 publications

(25 citation statements)

References 39 publications

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“…Xiao et al found that miR‐124 was significantly decreased in nasopharyngeal carcinoma (NPC) and that a miR‐124 mimic could inhibit NPC cell (CNE1 and CNE2) proliferation, migration, and invasion via binding with the target gene forkhead box Q1 (Foxq1) . In a recent study, miR‐124 inhibited TGF‐β‐induced cell proliferation and migration through SMAD and ERK‐related signaling pathways in NPC cells . Other research on cholangiocarcinoma (CCA) showed that miR‐124 could inhibit cell invasion and metastasis by targeting GATA6 .…”

Section: Mir‐124 and Other Malignant Tumorsmentioning

confidence: 99%

“…107 In a recent study, miR-124 inhibited TGF-β-induced cell proliferation and migration through SMAD and ERK-related signaling pathways in NPC cells. 108 Other research on cholangiocarcinoma (CCA) showed that miR-124 could inhibit cell invasion and metastasis by targeting GATA6. 109 In regard to gallbladder carcinoma, studies showed that miR-124 had a decreased expression level in clinical samples and cell lines (QBC939 and GBC-SD).…”

Section: Malignant Tumorsmentioning

confidence: 99%

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MicroRNA‐124: An emerging therapeutic target in cancer

et al. 2019

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MicroRNAs (miRNAs) are noncoding single‐stranded RNAs, approximately 20‐24 nucleotides in length, known as powerful posttranscriptional regulators. miRNAs play important regulatory roles in cellular processes by changing messenger RNA expression and are widely involved in human diseases, including tumors. It has been reported in the literature that miRNAs have a precise role in cell proliferation, programmed cell death, differentiation, and expression of coding genes. MicroRNA‐124 (miR‐124) has reduced exparession in various human neoplasms and is believed to be related to the occurrence, development, and prognosis of malignant tumors. In our review, we focus on the specific molecular functions of miR‐124 and the downstream gene targets in major cancers, which provide preclinical evidence for the treatment of human cancer. Although some obstacles exist, miR‐124 is still attracting intensive research focus as a promising and effective anticancer weapon.

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Section: Mir‐124 and Other Malignant Tumorsmentioning

confidence: 99%

Section: Malignant Tumorsmentioning

confidence: 99%

MicroRNA‐124: An emerging therapeutic target in cancer

et al. 2019

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“…Fan Y and colleagues showed that upregulation of MALAT1 promotes bladder cancer metastasis induced by TGF-β 31 . Wang Y et al 32 evaluated expression variation of MALAT1 after treated with TGF-β, finding that TGF-β significantly induced malat1 levels in human head and neck squamous cell carcinoma cells; subsequent similar work by Du MY et al 33 detected MALAT1 expression variation in 6-10B cells treated with TGF-β by way of qRT-PCR, showing that TGF-β treatment increased MALAT1 expression in nasopharyngeal carcinoma. The two independent studies fundamentally established the relationship between TGF-β1 and MALAT1 in outline; although the detailed regulation remains to be fleshed out with more data and evidence.…”

Section: Discussionmentioning

confidence: 95%

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

Liu¹,

Chen²,

Liu³

et al. 2020

J. Cancer

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Transforming growth factor β1 (TGF-β1) plays an important role in tumor initiation and development by inducing epithelial-mesenchymal Transition (EMT). Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) is a long noncoding RNA (lncRNA) that contributes to the invasion and metastasis of tumors, including esophageal squamous cell carcinoma (ESCC). The aim of the present study was to explore the underlying mechanisms implicated in EMT and to clarify whether TGF-β1 regulates MALAT1 expression, thereby promoting the invasion of ESCC. Expression of TGF-β1, MALAT1 and EMT-related markers, including E-cadherin and Vimentin, was detected in clinical samples of Kazakh's ESCC. The role of TGF-β1 in the regulation of MALAT1 in ESCC invasion was evaluated at the ESCC cell line level. High TGF-β1 expression was significantly associated with poor survival among patients with Kazakh's ESCC. Additionally, the expression of Vimentin was upregulated, and the expression of E-cadherin was downregulated and varied. The expression of MALAT1 positively correlated with the expression of TGF-β1 both in vivo and in vitro . Furthermore, knockdown of MALAT1 inhibited TGF-β1-induced EMT. Our data indicate that MALAT1 is heavily involved in EMT induced by TGF-β1. MALAT1 may be a therapeutic target in the suppression of metastasis and invasion of ESCC.

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“…Researchers found that SMAD4 plays a tumor suppressor role in many cancers, such as gastric cancer (GC), colorectal cancer, and cholangiocarcinoma . However, a large number of research showed that SMAD4, a significant factor in the TGF‐β/SMAD4 signaling pathway, plays a crucial part in signaling into the cell membrane and can contribute to the progression of EMT, Unfortunately, The specific role of SMAD4 in TGF‐β‐induced EMT in ESCC remains understudied. We provided evidence that knocking down of SMAD4 expression could partially reverse TGF‐induced EMT progression, increases E‐Cadherin protein expression, decreases N‐Cadherin and vimentin protein expression, and inhibits the invasion and migration of EC‐1 cells.…”

Section: Discussionmentioning

confidence: 99%

miR‐130a‐3p regulated TGF‐β1‐induced epithelial‐mesenchymal transition depends on SMAD4 in EC‐1 cells

Tian

Qian

et al. 2019

Cancer Medicine

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Metastasis and invasion are the primary causes of malignant progression in esophageal squamous cell carcinoma (ESCC). Epithelial‐mesenchymal transition (EMT) is crucial step of acquisition of "stemness" properties in tumor cells. However, the mechanism of esophageal cancer metastasis remains unclear. This research was designed to explore the role and mechanism of SMAD4 and miR‐130a‐3p in the progression of transforming growth factor‐β (TGF‐β)‐induced EMT in vivo and in vitro. The expression of miR‐130a‐3p in ESCC cell line and normal esophageal epithelial cell was determined by RT‐qPCR. The protein expression levels of TGF‐β‐induced changes in EMT were analyzed by western blotting and immunofluorescence. Dual‐luciferase report assays were used to validate the regulation of miR‐130a‐3p‐SMAD4 axis. The effect of miR‐130a‐3p and SMAD4 in TGF‐β‐induced migration, invasion in the ESCC cell line EC‐1 was investigated by wound healing assays and Transwell assays. Here we found that knocked down SMAD4 could partially reverse TGF‐β‐induced migration, invasion, and EMT progression in the ESCC cell line EC‐1. miR‐130a‐3p, which directly targets SMAD4, is down‐regulated in ESCC. miR‐130a‐3p inhibits the migration and invasion of EC‐1 cells both in vitro and in vivo. Finally, miR‐130a‐3p inhibits TGF‐β‐induced EC‐1 cell migration, invasion, and EMT progression in a SMAD4‐dependent way. In conclusion, this study provides new insights into the mechanism underlying ESCC metastasis. The TGF‐β/miR‐130a‐3p/SMAD4 pathway could be potential targets for clinical treatment of ESCC.

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TGF-β regulates the ERK/MAPK pathway independent of the SMAD pathway by repressing miRNA-124 to increase MALAT1 expression in nasopharyngeal carcinoma

Cited by 29 publications

References 39 publications

MicroRNA‐124: An emerging therapeutic target in cancer

MicroRNA‐124: An emerging therapeutic target in cancer

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

miR‐130a‐3p regulated TGF‐β1‐induced epithelial‐mesenchymal transition depends on SMAD4 in EC‐1 cells

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