miR‐22 and miR‐214 targeting BCL9L inhibit proliferation, metastasis, and epithelial‐mesenchymal transition by down‐regulating Wnt signaling in colon cancer

Sun, Ruifang; Liu, Zhigang; Lin, Han; Yang, Yang; Wu, Fei; Jiang, Qingwei; Zhang, Huahua; Ma, Ruili; Miao, Jiyu; He, Kang; Wang, Xiaofei; Zhou, Daohong; Huang, Chen

doi:10.1096/fj.201801798rr

Cited by 30 publications

(21 citation statements)

References 46 publications

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“…27 Besides, miR-214 sensitized CC cells to irradiation by suppression of ATG12-regulated autophagy. 28 Even though miR-214 was corroborated to inhibit CC tumor growth in nude mice, 29 its connection with metastasis in vivo remains unclear. Our microarray analysis revealed that miR-214 was one of the most significantly downregulated miRNAs in CC.…”

Section: Discussionmentioning

confidence: 99%

<p>SRF Potentiates Colon Cancer Metastasis and Progression in a microRNA-214/PTK6-Dependent Manner</p>

Li¹,

Wan²,

Su³

et al. 2020

CMAR

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Serum response factor (SRF), a sequence-specific transcription factor, is closely related to metastasis of gastric cancer, a digestive tract cancer. Herein, we probed the effect of SRF on metastasis and progression of colon cancer (CC), another digestive tract disorder, and the detailed mechanism. Methods: Microarray analysis was conducted on tumor and adjacent tissues to filter differentially expressed miRNA, followed by RT-qPCR validation in CC cell lines. The transcription factor and the target gene of microRNA-214 (miR-214) were predicted, and their binding relationships were tested by luciferase reporter assays and ChIP assays. Subsequently, SRF and protein tyrosine kinase 6 (PTK6) expression in CC patients and cells was evaluated by RT-qPCR, while JAK2 and STAT3 expression in cells by Western blot analysis. To further explore functions of miR-214, PTK6 and SRF on CC, CC cells were delivered with si-PTK6, miR-214 mimic and/or SRF overexpression. Results: miR-214 expressed poorly in CC tissues and cell lines, which related to advanced TNM staging and survival. miR-214 mimic inhibited proliferation, migration, invasion, xenograft tumor growth and metastasis of CC cells. SRF, overexpressed in CC samples and cells, suppressed the transcription of miR-214. Meanwhile, SRF upregulation counteracted the inhibitory role of miR-214 mimic in CC cell growth. miR-214 negatively regulated PTK6 expression to impair the JAK2/STAT3 pathway activation, thereby halting CC cell proliferation, migration, invasion, xenograft tumor growth and metastasis. Conclusion: Altogether, miR-214 may perform as a tumor suppressor in CC, and the SRF/ miR-214/PTK6/JAK2/STAT3 axis could be applied as a biomarker and potential therapeutic target.

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Section: Discussionmentioning

confidence: 99%

<p>SRF Potentiates Colon Cancer Metastasis and Progression in a microRNA-214/PTK6-Dependent Manner</p>

Li¹,

Wan²,

Su³

et al. 2020

CMAR

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“…It was also found that miR-214 significantly promoted the EMT process of melanoma, while CADM1 inhibited the EMT process. These results were similar to those of previous studies ( 46 – 48 ), thus indicating that miR-214 increased the invasion and migration of melanoma by downregulating CADM1 to promote the EMT process. However, it has also been revealed that miR-214 promotes cancer progression by activating the NF-κB signaling pathway ( 49 ).…”

Section: Discussionsupporting

confidence: 92%

MicroRNA‑214 promotes the EMT process in melanoma by downregulating CADM1 expression

Wang

Wen

et al. 2020

Mol Med Rep

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Melanoma is a malignant skin cancer type associated with a high mortality rate, but its treatment is currently not ideal. Both microrna (mir)-214 and cell adhesion molecule 1 (cadM1) are differentially expressed in melanoma, but their role in this cancer type remains unknown. Therefore, the aim of the present study was to investigate the role of cadM1 and mir-214 in melanoma to identify novel targets for its treatment. The expression levels of cadM1 and mir-214 in cells were detected by reverse transcription-quantitative Pcr (rT-qPcr). Moreover, cell viability, migration and invasion were measured by MTT, wound healing and Transwell assays, respectively. in addition, the relative expression levels of epithelial-mesenchymal transition (eMT)-related proteins in cells were detected by rT-qPcr and western blotting. it was found that the expression of cadM1 was inhibited in melanoma cells, while mir-214 expression was increased during melanoma tumorigenesis. Furthermore, mir-214 mimics promoted the viability, migration and invasion of melanoma cells. it was also demonstrated that the downregulation of cadM1 reversed the inhibitory effect of the mir-214 inhibitor in melanoma. Moreover, overexpression of cadM1 inhibited the eMT process in melanoma, while the mir-214 inhibitor suppressed the eMT process. The results also indicated that mir-214 promoted the eMT process by downregulating cadM1, which may represent a novel mechanism for the progression of melanoma.

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“…MiR-214-3p is involved in many pathological and physiological processes, such as cell growth, migration, proliferation, invasion, apoptosis, and fibrosis. 51,52 Our previous study also demonstrated that miR-214-3p plays an important role in regulating cardiac pyroptosis by binding to the caspase-1 during diabetic cardiomyopathy progression. 28 Moreover, consistent with the present study, our previous report has documented that the level of miR-214-3p is significantly decreased in patients with DM, 53 which is in agreement with the published data by other groups, 54,55 suggesting the possible implication of our findings in humans.…”

Section: Discussionmentioning

confidence: 91%

Melatonin exerts neuroprotective effects by inhibiting neuronal pyroptosis and autophagy in STZ‐induced diabetic mice

Che

Yang

et al. 2020

FASEB j.

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Diabetes mellitus (DM) patients are at a higher risk of developing brain injury characterized by neuronal death. Melatonin, a hormone produced by the pineal gland, exerts neuroprotective effects against brain damage. However, the effect of melatonin on diabetes‐induced brain injury has not been elucidated. This study was to evaluate the role of melatonin against neuronal death in DM and to elucidate the underlying mechanisms. Herein, we found that melatonin administration significantly alleviated the neuronal death in both streptozotocin (STZ)‐induced diabetic mice and high glucose (HG)‐treated neuronal cells. Melatonin inhibited neuronal pyroptosis and excessive autophagy, as evidenced by decreased levels of NLRP3, cleaved caspase‐1, GSDMD‐N, IL‐1β, LC3, Beclin1, and ATG12 both in vivo and in vitro. MicroRNA‐214‐3p (miR‐214‐3p) was decreased in DM mice and HG‐treated cells, and such a downregulation was corrected by melatonin, which was accompanied by repression of caspase‐1 and ATG12. Furthermore, downregulation of miR‐214‐3p abrogated the anti‐pyroptotic and anti‐autophagic actions of melatonin in vitro. Our results indicate that melatonin exhibits a neuroprotective effect by inhibiting neuronal pyroptosis and excessive autophagy through modulating the miR‐214‐3p/caspase‐1 and miR‐214‐3p/ATG12 axes, respectively, and it might be a potential agent for the treatment of brain damage in the setting of DM.

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miR‐22 and miR‐214 targeting BCL9L inhibit proliferation, metastasis, and epithelial‐mesenchymal transition by down‐regulating Wnt signaling in colon cancer

Cited by 30 publications

References 46 publications

<p>SRF Potentiates Colon Cancer Metastasis and Progression in a microRNA-214/PTK6-Dependent Manner</p>

<p>SRF Potentiates Colon Cancer Metastasis and Progression in a microRNA-214/PTK6-Dependent Manner</p>

MicroRNA‑214 promotes the EMT process in melanoma by downregulating CADM1 expression

Melatonin exerts neuroprotective effects by inhibiting neuronal pyroptosis and autophagy in STZ‐induced diabetic mice

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