MiR-143-5p Deficiency Triggers EMT and Metastasis by Targeting HIF-1α in Gallbladder Cancer

He, Min; Zhan, Ming; Chen, Wei; Xu, Sunwang; Long, Manmei; Shen, Hui; Shi, Yan-Hui; Liu, Qiang; Mohan, Man; Wang, Jian

doi:10.1159/000479903

Cited by 50 publications

(35 citation statements)

References 34 publications

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“…Activated Twist induces the up-regulation in N-cadherin and down-regulation in E-cadherin (46). Furthermore, miR-143-5p has been shown to exert an inhibitory effect on gallbladder cancer proliferation and metastasis by reducing the expression of HIF-1a, which further down-regulated Twist1 and impeded EMT process (47). Snail1 is a transcriptional repressor of E-cadherin that triggers EMT (48).…”

Section: Discussionmentioning

confidence: 99%

“…In order to further verify the binding activity of miR-143-5p to LAMP3 and HAGLR, RNA pull-down assay was performed. NC-bio-probe that could not be bound by LAMP3 and HAGLR was employed as the NC, with hypoxia-inducible factor (HIF)-1a, which has been previously confirmed to bind to miR-143-5p (29), serving as the positive control. In contrast to Mut-miR-143-5p, the enrichment of HAGLR and LAMP3 was remarkably elevated in WT-miR-143-5p (P , 0.05), indicating direct binding between miR-143-5p and HAGLR as well as a direct binding between LAMP3 and miR-143-5p (Fig.…”

Section: Ec Tissues Exhibit Enhanced Epithelial-mesenchymal Transitionmentioning

confidence: 99%

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Long noncoding RNA HAGLR acts as a microRNA‐143‐5p sponge to regulate epithelial‐mesenchymal transition and metastatic potential in esophageal cancer by regulating LAMP3

et al. 2019

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Homeobox D gene cluster antisense growth‐associated long noncoding RNA (HAGLR) functions as a crucial regulator in the progression and development of human cancers. We analyzed effects of HAGLR, microRNA (miR)‐143‐5p and lysosome‐associated membrane glycoprotein (LAMP)3 on esophageal cancer (EC) and the related mechanisms. Microarray analysis was used to screen out EC‐related genes and the regulation network among HAGLR, miR‐143‐5p, and LAMP3. The regulatory mechanisms of HAGLR and miR‐143‐5p in EC were analyzed following the treatment of miR‐143‐5p mimic, miR‐143‐5p inhibitor, HAGLR vector, or small interfering RNA against HAGLR in EC cells. The expression of N‐cadherin, vimentin, Twist1, Snail1, and E‐cadherin as well as the abilities of cell proliferation, invasion, and migration were measured. The effects of the HAGLR/miR‐143‐5p/LAMP3 axis were determined in vivo by assessing tumor formation in nude mice. The expression of HAGLR and LAMP3 was increased, whereas that of miR‐143‐5p was diminished in EC tissues and cells. HAGLR could competitively bind to miR‐143‐5p, and miR‐143‐5p targeted LAMP3. Down‐regulated HAGLR or up‐regulated miR‐143‐5p increased E‐cadherin expression and significantly diminished expression of LAMP3, N‐cadherin, vimentin, Twist1, and Snail1. Moreover, down‐regulated HAGLR inhibited cell proliferation, invasion, migration, epithelial‐mesenchymal transition (EMT), and tumor growth. Moreover, down‐regulation of HAGLR inhibited LAMP3 expression by sponging miR‐143‐5p, thereby suppressing the progression of EC. Taken together, our results suggest HAGLR acts as a competing endogenous RNA of miR‐143‐5p to increase the expression of LAMP3, thus promoting EMT, proliferation, invasion, and migration in EC cells.—Yang, C., Shen, S., Zheng, X., Ye, K., Sun, Y., Lu, Y., Ge, H. Long noncoding RNA HAGLR acts as a microRNA‐143‐5p sponge to regulate epithelial‐mesenchymal transition and metastatic potential in esophageal cancer by regulating LAMP3. FASEB J. 33, 10490–10504 (2019). http://www.fasebj.org

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Section: Discussionmentioning

confidence: 99%

Section: Ec Tissues Exhibit Enhanced Epithelial-mesenchymal Transitionmentioning

confidence: 99%

Long noncoding RNA HAGLR acts as a microRNA‐143‐5p sponge to regulate epithelial‐mesenchymal transition and metastatic potential in esophageal cancer by regulating LAMP3

et al. 2019

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“…Moreover, miR-143-5p deficiency in gallbladder cancer triggered the EMT and metastasis by targeting HIF-1α in mesothelioma. 27 miR-143-3p suppresses the progression of ovarian cancer and esophageal squamous cell carcinoma, 28 , 29 and miR-145-3p acts as a tumor suppressor in HNSCC by targeting MYO1B . 30 Despite some evidence that miRNAs in the 143/145 group may be co-regulated, 31 in the context of the current work, we did not evaluate the expression of miRNAs other than miR-145-5p, given our focus on FSCN1 .…”

Section: Discussionmentioning

confidence: 99%

Promoter Methylation-Regulated miR-145-5p Inhibits Laryngeal Squamous Cell Carcinoma Progression by Targeting FSCN1

Gao

Zhang

et al. 2019

Molecular Therapy

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Laryngeal squamous cell carcinoma (LSCC) is a common form of head and neck cancer with poor prognosis. However, the mechanism underlying the pathogenesis of LSCC remains unclear. Here, we demonstrated increased expression of fascin actin-bundling protein 1 ( FSCN1 ) and decreased expression of microRNA-145-5p (miR-145-5p) in a clinical cohort of LSCC. Luciferase assay revealed that miR-145-5p is a negative regulator of FSCN1 . Importantly, low miR-145-5p expression was correlated with TNM (tumor, node, metastasis) status and metastasis. Moreover, cases with low miR-145-5p/high FSCN1 expression showed poor prognosis, and these characteristics together served as independent prognostic indicators of survival. Gain- and loss-of-function studies showed that miR-145-5p overexpression or FSCN1 knockdown inhibited LSCC migration, invasion, and growth by suppressing the epithelial-mesenchymal transition along with inducing cell-cycle arrest and apoptosis. Additionally, hypermethylation of the miR-145-5p promoter suggested that repression of miR-145-5p arises through epigenetic inactivation. LSCC tumor growth in vivo could be inhibited by using miR-145-5p agomir or FSCN1 small interfering RNA (siRNA), which highlights the potential for clinical translation. Collectively, our findings indicate that miR-145-5p plays critical roles in inhibiting the progression of LSCC by suppressing FSCN1 . Both miR-145-5p and FSCN1 are important potential prognostic markers and therapeutic targets for LSCC.

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“…12 Epithelial-interstitial transformation (EMT) is a process in which epithelial cells lose their original polarity, thus obtaining anti-apoptosis, high migration, and invasion ability, and transforming into interstitial cells. 22 However, the occurrence of DDR1 and EMT is also closely related. Reports 23 once showed that the upregulation of DDR1 can promote the development of colorectal cancer by reducing the expression of E-Cadherin.…”

Section: Discussionmentioning

confidence: 99%

<p>Promotion of miR-221-5p on the Sensitivity of Gastric Cancer Cells to Cisplatin and Its Effects on Cell Proliferation and Apoptosis by Regulating DDR1</p>

Jiang

Guo

et al. 2020

OTT

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Purpose: This research aimed to explore the role of miR-221-5p on the sensitivity of gastric cancer cells to cisplatin, and the proliferation and invasion of gastric cancer cells by regulating DDR1. Patients and Methods: Altogether 69 patients who treated with radical gastrectomy from January 2014 to January 2016 were collected. With the agree of the patients, 69 gastric carcinoma and 69 adjacent tissues were taken, respectively, during the operation, and gastric carcinoma and human gastric mucosa cells were purchased. RT-PCR was used for detection of the expression level of miR-221-5p and DDR1. Wound healing assay and CCK-8 assay were used for exploration of the cell migration and viability. Western blot and double luciferase reporter gene were performed to determine the target gene of miR-221-5p. Results: It was showed that miR-221-5p expression was decreased in GC tissues and cell lines. The high expression of miR-221-5p reduced the resistance of GC cells to cisplatin and inhibited the proliferation and migration of gastric cancer cells. The high expression of miR-221-5p promoted the proliferation, invasion and migration of GC cells. In addition, we found that DDR1 was a direct target gene of miR-221-5p in GC cells. We found that DDR1 expression increased in gastric carcinoma. Moreover, there was a negative correlation of DDR1 with the expression level of miR-221-5p. The increase of miR-221-5p increased the chemosensitivity of GC cells to cisplatin, and inhibited the proliferation, invasion, migration and EMT of GC cells by targeting DDR1. Conclusion: The above research indicated that miR-221-5p may be a target for enhancing cisplatin chemotherapy sensitivity in gastric cancer patients.

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MiR-143-5p Deficiency Triggers EMT and Metastasis by Targeting HIF-1α in Gallbladder Cancer

Cited by 50 publications

References 34 publications

Long noncoding RNA HAGLR acts as a microRNA‐143‐5p sponge to regulate epithelial‐mesenchymal transition and metastatic potential in esophageal cancer by regulating LAMP3

Long noncoding RNA HAGLR acts as a microRNA‐143‐5p sponge to regulate epithelial‐mesenchymal transition and metastatic potential in esophageal cancer by regulating LAMP3

Promoter Methylation-Regulated miR-145-5p Inhibits Laryngeal Squamous Cell Carcinoma Progression by Targeting FSCN1

<p>Promotion of miR-221-5p on the Sensitivity of Gastric Cancer Cells to Cisplatin and Its Effects on Cell Proliferation and Apoptosis by Regulating DDR1</p>

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