miR‑28‑5p inhibits the migration of breast�cancer by regulating WSB2

Ma, Liang; Zhang, Yunfeng; Hu, Fang

doi:10.3892/ijmm.2020.4685

Cited by 16 publications

(15 citation statements)

References 27 publications

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“…In this study, we identified TUC338 as a cytoplasmic lncRNA in DLBCL cells that could sponge miR-28-5p and inhibit its activity. miR-28-5p is a well-documented tumor suppressor in various cancer types, including breast cancer [ 25 ], pancreatic cancer [ 26 , 27 ], endometrial cancer [ 28 ], colorectal cancer [ 29 ], and hepatocellular carcinoma [ 30 ]. Here, we found that miR-28-5p level was significantly decreased in human DLBCL tissues, and silencing of miR-28-5p could effectively block the decreased cell malignant phenotype caused by TUC338 knockdown, suggesting that miR-28-5p also plays a tumor-inhibiting role in DLBCL.…”

Section: Discussionmentioning

confidence: 99%

TUC338 Promotes Diffuse Large B Cell Lymphoma Growth via Regulating EGFR/PI3K/AKT Signaling Pathway

Jia

Zhao

et al. 2021

Journal of Oncology

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TUC338 is emerging as a novel vital long noncoding RNA (lncRNA) in human cancer; however, its role in diffuse large B cell lymphoma (DLBCL) remains unknown. In this study, we found that TUC338 was remarkably upregulated in DLBCL tissues as compared to matched normal tissues. High TUC338 was closely related to advanced Ann Arbor stage, resistance to CHOP-like treatment, and high IPI (International Prognostic Index). Stable knockdown of TUC338 evidently inhibited cell proliferation and chemotherapy resistance to Adriamycin and induced apoptosis. Further, we found that TUC338 was able to directly bind to miR-28-5p and increased EGFR level, resulting in activating carcinogenic PI3K/AKT signaling, thereby facilitating DLBCL uncontrolled growth. Moreover, we also found that depletion of TUC338 led to the inactivation of EGFR/PI3K/AKT pathway in vivo by using the xenograft tumor model. Preclinically, DLBCL patients with high TUC338 had shorter survival time than those with low TUC338, and serum TUC338 level was identified as an excellent indicator for DLBCL diagnosis. In sum, our findings clearly indicate that TUC338 functions as an oncogenic lncRNA in DLBCL through activating EGFR/PI3K/AKT pathway via sponging and inhibiting miR-28-5p, which may be a promising target for DLBCL treatment.

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Section: Discussionmentioning

confidence: 99%

TUC338 Promotes Diffuse Large B Cell Lymphoma Growth via Regulating EGFR/PI3K/AKT Signaling Pathway

Jia

Zhao

et al. 2021

Journal of Oncology

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“…Compared with that in human breast epithelial cells (HMECs), the expression of miR‐28‐5p in breast cancer cells was significantly decreased. Transfection of miR‐28‐5p mimics could inhibit the migration of MCF‐7 cells, whereas miR‐28‐5p inhibitors had the opposite effect (Ma et al, 2020). Furthermore, CRC was reported to be negatively regulated by miR‐28‐5p (Fan et al, 2020), and insulin‐like growth factor‐1 (IGF‐1) mediated the downregulation of miR‐28‐5p expression in human hepatocellular carcinoma (HCC) (Shi & Teng, 2015).…”

Section: Discussionmentioning

confidence: 99%

A nontoxic dose of chrysotile can malignantly transform Met‐5A cells, in which microRNA‐28 has inhibitory effects

Zhang

Yuan

Sun

et al. 2021

J of Applied Toxicology

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Chrysotile, which is classified as a class I carcinogen by the International Agency for Research on Cancer (IARC), has extensive application in the industry and can lead to lung or other cancers. However, whether chrysotile causes malignant mesothelioma and its molecular mechanism remain debatable. Thus, this study aimed to demonstrate the mesothelioma‐inducing potential of chrysotile at the mesothelial cellular level and the function of microRNA‐28 in malignantly transformed mesothelial MeT‐5A cells. MeT‐5A cells malignantly transformed by a nontoxic dose of chrysotile were named Asb‐T, and miR‐28 expression was downregulated in Asb‐T cells. Restoration of miR‐28 expression inhibited the proliferation, migration and invasion of Asb‐T cells. We verified that IMPDH is a putative target of miR‐28. The expression of IMPDH was significantly higher in Asb‐T MeT‐5A cells than in control cells, whereas the opposite trend was observed with miR‐28 overexpression. Additionally, inhibition of IMPDH had similar effects as miR‐28 overexpression. After miR‐28 was elevated or IMPDH was inhibited, Ras activation was reduced, and its downstream pathways (the Erk and Akt signalling pathways) were inhibited. Surprisingly, the content of miR‐28 in the blood of mesothelioma patients was higher than that in control subjects. Overall, nontoxic doses of chrysotile can cause malignant transformation of MeT‐5A cells. Moreover, miR‐28 inhibits the proliferation, migration and invasion of Asb‐T MeT‐5A cells, negatively regulates the expression of IMPDH through the Ras signalling pathway and may be an important therapeutic target.

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“…miRNAs are involved in various viral infectious diseases, such as human immunodeficiency virus-1 (HIV-1) infection (19), human papillomavirus infection (20), SARS-CoV infection (21) and hepatitis B virus infection (20)(21)(22). As mature miRNAs, miR-28-3p and miR-28-5p are derived from the 3' and 5' ends, respectively, of pre-miR-28 and then go on to target different mRNAs, such as WD repeat and SOCS box-containing 2 and forkhead box O1 (23)(24)(25)(26)(27). There is evidence indicating that miRNAs may block RNA virus replication during viral infection (28).…”

Section: Microrna-28-3p Inhibits Angiotensin-converting Enzymementioning

confidence: 99%

MicroRNA‑28‑3p inhibits angiotensin‑converting enzyme 2 ectodomain shedding in 293T cells treated with the spike protein of severe acute respiratory syndrome coronavirus 2 by targeting A disintegrin and metalloproteinase 17

Yun

2021

Int J Mol Med

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the virus that causes coronavirus disease 2019. Angiotensin-converting enzyme 2 (ACE2) is the SARS-CoV binding site and is ubiquitously expressed in endothelial cells of several organs, with the highest levels in the cardiovascular system, kidney and lungs. A disintegrin and metalloproteinase 17 (ADAM17) is involved in ectodomain shedding of ACE2. In the present study, reverse-transcription-quantitative PCR, transfection, TUNNEL assay, dual-luciferase activity assay and western blotting were conducted to investigate the effects of microRNA (miR)-28-3p on ADAM17-dependent shedding of the ACE2 ectodomain following treatment with the spike protein (S-protein) of SARS-CoV-2. It was found that miR-28-3p was significantly downregulated in 293T cells treated with 100 ng/ml of S-protein for 24 h at 37˚C, which led to upregulation of ADAM17. In addition, the expression of ADAM17 and miR-28-3p were negatively correlated based on Pearson's correlation test in 293T cells treated with S-protein for 24 h. Overexpression of miR-28-3p and inhibition of ADAM17 regulated 293T cell viability, apoptosis and ACE2 ectodomain shedding. It was also demonstrated that ADAM17 was the target gene of miR-28-3p and that miR-28-3p negatively regulated ADAM17 expression. Notably, the inhibition of ADAM17 expression blocked the effects of miR-28-3p inhibitor on proliferation, apoptosis and ACE2 ectodomain shedding in 293T cells treated with S-protein.The findings of the present study suggested that miR-28-3p inhibits ADAM17-dependent ACE2 ectodomain shedding in 293T cells treated with the S-protein of SARS-CoV-2, which suggested the potential therapeutic role of miR-28-3p mimic in the prevention and treatment of patients with SARS-CoV-2.

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miR‑28‑5p inhibits the migration of breast�cancer by regulating WSB2

Cited by 16 publications

References 27 publications

TUC338 Promotes Diffuse Large B Cell Lymphoma Growth via Regulating EGFR/PI3K/AKT Signaling Pathway

TUC338 Promotes Diffuse Large B Cell Lymphoma Growth via Regulating EGFR/PI3K/AKT Signaling Pathway

A nontoxic dose of chrysotile can malignantly transform Met‐5A cells, in which microRNA‐28 has inhibitory effects

MicroRNA‑28‑3p inhibits angiotensin‑converting enzyme 2 ectodomain shedding in 293T cells treated with the spike protein of severe acute respiratory syndrome coronavirus 2 by targeting A disintegrin and metalloproteinase 17

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