MiR-27b-3p exerts tumor suppressor effects in esophageal squamous cell carcinoma by targeting Nrf2

Han, Mei; Li, Na; Li, Fanzhou; Wang, Hua; Ma, Lifang

doi:10.1007/s13577-020-00329-7

Cited by 26 publications

(26 citation statements)

References 32 publications

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“…Thus, infiltration and metastasis may be the leading causes of deterioration and poor prognosis in CSCC. miR-27b-3p, which exhibits anticancer effects, is downregulated in several types of cancer, such as breast cancer, lung carcinoma, esophageal carcinoma and colorectal carcinoma (14,(23)(24)(25). Han et al (24) determined that miR-27b-3p was downregulated in esophageal squamous cell carcinoma (ESCC) tissue samples and cell lines and was associated with poor cell differentiation, TNM staging and lymphatic metastasis.…”

Section: Discussionmentioning

confidence: 99%

“…miR-27b-3p, which exhibits anticancer effects, is downregulated in several types of cancer, such as breast cancer, lung carcinoma, esophageal carcinoma and colorectal carcinoma (14,(23)(24)(25). Han et al (24) determined that miR-27b-3p was downregulated in esophageal squamous cell carcinoma (ESCC) tissue samples and cell lines and was associated with poor cell differentiation, TNM staging and lymphatic metastasis. The transcription factor nuclear-related factor 2 is the direct target of miR-27b-3p, as evidenced by dual-luciferase reporter assays (24).…”

Section: Discussionmentioning

confidence: 99%

“…Han et al (24) determined that miR-27b-3p was downregulated in esophageal squamous cell carcinoma (ESCC) tissue samples and cell lines and was associated with poor cell differentiation, TNM staging and lymphatic metastasis. The transcription factor nuclear-related factor 2 is the direct target of miR-27b-3p, as evidenced by dual-luciferase reporter assays (24). In a study conducted by Zeng et al (26), IL-10 induced the upregulation of miR-27b-3p and reduced the mRNA stability of proliferating cell nuclear antigen, which inhibited the development of hemangioma cavernosum.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA‑27b‑3p inhibits the proliferation and invasion of cutaneous squamous cell carcinoma by targeting EGFR and MMP‑13

Liang

Zhang

2021

Oncol Lett

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Cutaneous squamous cell carcinoma is a common malignant tumor. The aim of the present study was to examine the biological function of microRNA (miR)-27b-3p in cutaneous squamous cell carcinoma (CSCC) and its underlying mechanism. The relative expression levels of miR-27b-3p were determined in A-431, Colo-16 and NHEK/SVTERT3-5 cell lines. The regulatory effects of miR-27b-3p on the proliferation of CSCC cells were evaluated using MTT and colony formation assays. Transwell assays were conducted to examine the role of miR-27b-5p in the migratory and invasive abilities of CSCC cells. The levels of EGFR, MMP-13, Akt, phosphorylated (p)-Akt, cyclin D1, N-cadherin (CAD) and E-CAD were detected in CSCC cells using reverse transcription-quantitative PCR and western blot analysis. Binding between miR-27b-3p and the 3'-untranslated region (UTR) of EGFR or MMP-13 was assessed using a dual-luciferase reporter assay. miR-27b-3p was significantly downregulated in CSCC cell lines, compared with the skin keratinocyte cell line. Transfection with a miR-27b-3p mimic significantly reduced the proliferative, migratory and invasive abilities of CSCC cells in vitro. Moreover, miR-27b-3p mimic transfection downregulated the mRNA and protein levels of EGFR, MMP-13, cyclin D1, p-Akt and N-CAD, whilst upregulating E-CAD levels in CSCC cells. miR-27b-3p was found to target the EGFR and MMP-13 3'-UTRs, thus downregulating the expression of these molecules. The inhibition of CSCC proliferation by miR-27b-3p was effectively reversed by EGFR overexpression. Moreover, the inhibitory effect of miR-27b-3p on the migratory and invasive abilities of CSCC cells was abolished by MMP-13 overexpression. In conclusion, miR-27b-3p inhibits the proliferation, migration and invasion of CSCC cells by downregulating the expression of EGFR and MMP-13 and may represent a potential diagnostic marker and therapeutic option for CSCC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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MicroRNA‑27b‑3p inhibits the proliferation and invasion of cutaneous squamous cell carcinoma by targeting EGFR and MMP‑13

Liang

Zhang

2021

Oncol Lett

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“…Due to the multi-target gene characteristics of microRNAs, we can speculate that miR-27b-3p may play different role in different environments and different cells. Despite studies has reported that low expression of miR-27b-3p was related to chemoresistance in various cancer cell lines [34][35][36], miR-27b-3p was still found playing a as a tumor suppressor in GC [31], breast cancer [29], lung cancer [37], glioma [38], and esophageal squamous cell carcinoma [39]. Of note, the mechanisms of autophagy inhibition by hsa_circ_0006470 and its interaction with other potential microRNAs during GC development deserve further elucidations.…”

Section: Discussionmentioning

confidence: 98%

circRNA_0006470 promotes the proliferation and migration of gastric cancer cells by functioning as a sponge of miR-27b-3p

Cui¹,

Cao²,

Huang³

et al. 2021

neo

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Cancer pathogenesis is influenced by epigenetic alterations mediated by circular RNAs (circRNAs).In this study, we aimed to investigate the regulatory mechanisms and cytological function of hsa_circ_0006470/miR-27b-3p in gastric cancer (GC). CircRNA and microRNA expression in cancer cells were measured by the qRT-PCR method. A dual-luciferase reporter assay was performed to validate the binding of hsa_circ_0006470 with miR-27b-3p. hsa_circ_0006470 was silenced in AGS cells, and proliferation, migration, and invasion were tested via the CCK-8 assay and Transwell system, respectively. The autophagy in GC cells was assessed by marker protein detection and transmission electron microscope. The results showed that hsa_circ_0006470 expression was significantly elevated in GC cells, which was mainly distributed in cytoplasmic components and could directly bind with miR-27b-3p in GC cells. Silencing of hsa_circ_0006470 repressed cell proliferation, migration, and invasion, which may be through regulating miR-27b-3p/Receptor tyrosine kinase-like orphan receptor 1 (ROR1). Silencing of hsa_circ_0006470 also elevated LC3II and Beclin-1 and suppressed p62 protein abundances, which subsequently induced autophagy in AGS cells. Furthermore, we found that hsa_circ_0006470 promotes phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PI3KCA) expressing by sponging miR-27b-3p. In conclusion, hsa_circ_0006470 promoted GC cell proliferation and migration through targeting miR-27b-3p and suppressing autophagy machinery.

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“…We hypothesized that this may be related to the effect of Nrf2 expression. It has been reported that Nrf2 nuclear translocation could activate Notch1/Snail signaling pathway, which accelerated EMT and metastasis of tumor cells ( Han et al, 2020 ). In addition, PDCD4 inhibits the EMT pathway in tumors by increasing Keap1 expression and decreasing the level and activity of Nrf2 ( Hwang, Jeong & Chang, 2020 ), our study also found that Keap1 knockdown promoted Nrf2 nuclear translocation.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Kelch-like epichlorohydrin-related protein 1 promotes the progression and drug resistance of lung adenocarcinoma

Gao

Tang

et al. 2021

PeerJ

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Background Lung cancer is a common malignant carcinoma of respiratory system with high morbidity and mortality. Kelch-like epichlorohydrin-related protein 1 (Keap1), a member of the BTB-Kelch protein family, has been reported as an important molecule in several cancers. However, its potential role in tumor is still controversial. Here we aim to clarify the effect of Keap1 on the biological characteristics and chemotherapy resistance in lung adenocarcinoma (LUAD). Methods Immunohistochemistry was conducted to compare Keap1 expression in lung adenocarcinoma tissues and matched non-cancerous tissues, and the correlation between Keap1 expression and clinicopathological features was analyzed. Subsequently, the stable A549 and H1299 cell lines with Keap1 knockdown or overexpression were constructed using lentivirus. The roles of Keap1 on the cell proliferation, migration, invasion and drug resistance were investigated by colony formation assay, cell proliferation assay, wound scratch test, transwell invasion assay and drug sensitivity assay, respectively. Results Keap1 was lowly expressed in tumor tissues compared to matched non-cancerous tissues, and its expression was correlated with TNM stage and lymph node metastasis. Early stage (I) tumors without lymph node metastasis had higher levels of Keap1 expression compared with late-stage tumors (II, III) with the presence of lymphatic metastasis. Colony formation assays showed that Keap1 knockdown promoted the proliferation of A549 and H1299 cells, and the cell growth curves further confirmed this feature. In contrast, wound scratch and transwell invasion experiments showed that Keap1 overexpression inhibited cell migration and invasive malignancy. The IC50 for cisplatin and paclitaxel were significantly increased by Keap1 knockdown in A549 and H1299 cell lines. Conclusion Keap1 knockdown promotes tumor cell growth, proliferation, invasion, metastasis and chemotherapy resistance in LUAD. It may be a potential tumor marker to guide the staging and treatment of lung cancer.

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MiR-27b-3p exerts tumor suppressor effects in esophageal squamous cell carcinoma by targeting Nrf2

Cited by 26 publications

References 32 publications

MicroRNA‑27b‑3p inhibits the proliferation and invasion of cutaneous squamous cell carcinoma by targeting EGFR and MMP‑13

MicroRNA‑27b‑3p inhibits the proliferation and invasion of cutaneous squamous cell carcinoma by targeting EGFR and MMP‑13

circRNA_0006470 promotes the proliferation and migration of gastric cancer cells by functioning as a sponge of miR-27b-3p

Inhibition of Kelch-like epichlorohydrin-related protein 1 promotes the progression and drug resistance of lung adenocarcinoma

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