miR-30d-5p represses the proliferation, migration, and invasion of lung squamous cell carcinoma via targeting <i>DBF4</i>

Qi, Yitian; Hou, Yi; Qi, Liangchen

doi:10.1080/26896583.2021.1926855

Cited by 9 publications

(6 citation statements)

References 35 publications

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“…Studies have shown that miR-30d-5p is closely related to a variety of human tumors such as lung cancer (39), colorectal cancer (40), prostate cancer (41) and breast cancer (42), re ecting the important role of miR-30d-5p in tumor prognosis. miR-30d-5p can act both as an inhibitor that hinders tumor development (43) and as a promoter that accelerates tumorigenesis (44). In addition, miR-30d-5p also plays an important role in cell proliferation (45), migration(46), apoptosis (47), autophagy(48), tumorigenesis (49), and chemotherapy resistance (50).…”

Section: Discussionmentioning

confidence: 99%

The antimicrobial peptide Merecidin Inhibit the metastasis of triple-negative breast cancer by obstructing EMT via miR-30d-5p/vimentin

song,

ma,

et al. 2023

Preprint

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LL-37 is an important innate immune effector molecule with great potential in antitumor therapy. Merecidin retains the most active active fragment in LL-37 with antitumor biological activity and stability. This study mainly explores the inhibitory effect of antimicrobial peptide Merecidin on triple-negative breast cancer (TNBC) cells and the mechanism of inhibiting the epithelial-mesenchymal transition (EMT) by regulating miR-30d-5p/vimentin, thereby inhibiting breast cancer metastasis. The results showed that the Merecidin was able to inhibit the proliferation, migration and invasion capacity and EMT of TNBC cells (MDA-MB-231 and MDA-MB-468) in vitro. Laser confocal localization showed that Merecidin was mainly localized in the cytoplasm of TNBC cells, and the RT-qPCR results showed that miR-30d-5p was poorly expressed in TNBC cells, and Merecidin could significantly upregulate the expression of miR-30d-5p. In addition, the Dual-luciferase reporter and q-PCR results confirmed that miR-30d-5p binds to vimentin and negatively regulates vimentin. At the same time, pull down experiments showed that Merecidin can bind to vimentin in vitro. In addition, scratch experiments and Transwell experiments showed that miR-30d-5p inhibited the migration and invasion ability of TNBC cells, while vimentin promoted the migration and invasion ability of TNBC cells. Finally, down-regulation of miR-30d-5p or overexpression of vimentin could partially counteract the inhibitory effect of Merecidin on TNBC cell migration, invasion ability and EMT. In the nude mouse MDA-MB-231 subcutaneous tumor model, Merecidin significantly inhibited tumor growth and cell proliferation and upregulated the expression of miR-30d-5p in tumor tissues, inhibiting the expression of vimentin and EMT. In conclusion, Merecidin can effectively inhibit the proliferation, migration and invasion ability of TNBC cancer cells; localization in the cytoplasm; By regulating miR-30d-5p/vimentin, it can effectively hinder the EMT process, thereby effectively inhibiting the migration and invasion of TNBC cells. These findings provide new insights into the molecular function of Merecidin, suggesting its potential as a therapeutic agent for TNBC.

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Section: Discussionmentioning

confidence: 99%

The antimicrobial peptide Merecidin Inhibit the metastasis of triple-negative breast cancer by obstructing EMT via miR-30d-5p/vimentin

song,

ma,

et al. 2023

Preprint

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“…GOLGA8B knockdown inhibits cell invasion by suppressing the STAT3 signaling pathway in lung squamous cell carcinoma [ 36 ]. Down-regulation of miR-30d-5p promotes the proliferation, migration, and invasion of lung squamous cell carcinoma [ 37 ]. RUNX2 regulates expression of genes important in tumor cell migration, and has a role in cell proliferation and metastasis of lung cancer [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

The Oncogenic and Tumor Suppressive Long Non-Coding RNA–microRNA–Messenger RNA Regulatory Axes Identified by Analyzing Multiple Platform Omics Data from Cr(VI)-Transformed Cells and Their Implications in Lung Cancer

2022

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Chronic exposure to hexavalent chromium (Cr(VI)) causes lung cancer in humans, however, the underlying mechanism has not been well understood. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) are commonly studied non-coding RNAs. miRNAs function mainly through interaction with the 3′-untranslated regions of messenger RNAs (mRNAs) to down-regulate gene expression. LncRNAs have been shown to function as competing endogenous RNAs (ceRNAs) to sponge miRNAs and regulate gene expression. It is now well accepted that lncRNAs and miRNAs could function as oncogenes or tumor suppressors. Dysregulations of lncRNAs and miRNAs have been shown to play important roles in cancer initiation, progression, and prognosis. To explore the mechanism of Cr(VI) lung carcinogenesis, we performed lncRNA, mRNA, and miRNA microarray analysis using total RNAs from our previously established chronic Cr(VI) exposure malignantly transformed and passage-matched control human bronchial epithelial BEAS-2B cells. Based on the differentially expressed lncRNAs, miRNAs, and mRNAs between the control (BEAS-2B-Control) and Cr(VI)-transformed (BEAS-Cr(VI)) cells and by using the lncRNA–miRNA interaction and miRNA target prediction algorithms, we identified three oncogenic (HOTAIRM1/miR-182-5p/ERO1A, GOLGA8B/miR-30d-5p/RUNX2, and PDCD6IPP2/miR-23a-3p/HOXA1) and three tumor suppressive (ANXA2P1/miR-20b-5p/FAM241A (C4orf32), MIR99AHG/miR-218-5p/GPM6A, and SH3RF3-AS1/miR-34a-5p/HECW2) lncRNA–miRNA–mRNA regulatory axes. Moreover, the relevance of these three oncogenic and three tumor suppressive lncRNA–miRNA–mRNA regulatory axes in lung cancer was explored by analyzing publicly available human lung cancer omics datasets. It was found that the identified three oncogenic lncRNA–miRNA–mRNA regulatory axes (HOTAIRM1/miR-182-5p/ERO1A, GOLGA8B/miR-30d-5p/RUNX2, and PDCD6IPP2/miR-23a-3p/HOXA1) and the three tumor suppressive lncRNA–miRNA–mRNA regulatory axes (ANXA2P1/miR-20b-5p/FAM241A (C4orf32), MIR99AHG/miR-218-5p/GPM6A, and SH3RF3-AS1/miR-34a-5p/HECW2) have significant diagnostic and prognosis prediction values in human lung cancer. In addition, our recent studies showed that Cr(VI)-transformed cells display cancer stem cell (CSC)-like properties. Further bioinformatics analysis identified the oncogenic lncRNA–miRNA–mRNA regulatory axes as the potential regulators of cancer stemness. In summary, our comprehensive analysis of multiple platform omics datasets obtained from Cr(VI)-transformed human bronchial epithelial cells identified several oncogenic and tumor suppressive lncRNA–miRNA–mRNA regulatory axes, which may play important roles in Cr(VI) carcinogenesis and lung cancer in general.

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“…Interestingly, the content of miR-30d-5p varied between different grades of NSCLC, indicating that miR-30d-5p was associated with the occurrence and progression of NSCLC (Xue et al, 2021;Zhao et al, 2021). In addition, Qi et al indicated that the expression of miR-30d-5p in LUSC cells was significantly downregulated, and the proliferation, migration and invasion of tumor cells were subsequently reduced, indicating that miR-30d-5p had a clear antitumor effect (Qi et al, 2021). Luciferase experiments also verified the targeted binding of miR-30d-5p with DBF4's 3′-UTR region, which inhibited various physiological functions of cancer cells (Qi et al, 2021).…”

Section: Lung Cancermentioning

confidence: 99%

miR-30d-5p: A Non-Coding RNA With Potential Diagnostic, Prognostic and Therapeutic Applications

Zhao

Yuan

Zheng

et al. 2022

Front. Cell Dev. Biol.

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Cancer is a great challenge facing global public health. Scholars have made plentiful efforts in the research of cancer therapy, but the results are still not satisfactory. In relevant literature, the role of miRNA in cancer has been widely concerned. MicroRNAs (miRNAs) are a non-coding, endogenous, single-stranded RNAs that regulate a variety of biological functions. The abnormal level of miR-30d-5p, a type of miRNAs, has been associated with various human tumor types, including lung cancer, colorectal cancer, esophageal cancer, prostate cancer, liver cancer, cervical cancer, breast cancer and other types of human tumors. This reflects the vital function of miR-30d-5p in tumor prognosis. miR-30d-5p can be identified either as an inhibitor hindering the development of, or a promoter accelerating the occurrence of tumors. In addition, the role of miR-30d-5p in cell proliferation, motility, apoptosis, autophagy, tumorigenesis, and chemoresistance are also noteworthy. The multiple roles of miR-30d-5p in human cancer suggest that it has broad feasibility as a biomarker and therapeutic target. This review describes the connection between miR-30d-5p and the clinical indications of tumors, and summarizes the mechanisms by which miR-30d-5p mediates cancer progression.

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miR-30d-5p represses the proliferation, migration, and invasion of lung squamous cell carcinoma via targeting DBF4

Cited by 9 publications

References 35 publications

The antimicrobial peptide Merecidin Inhibit the metastasis of triple-negative breast cancer by obstructing EMT via miR-30d-5p/vimentin

The antimicrobial peptide Merecidin Inhibit the metastasis of triple-negative breast cancer by obstructing EMT via miR-30d-5p/vimentin

The Oncogenic and Tumor Suppressive Long Non-Coding RNA–microRNA–Messenger RNA Regulatory Axes Identified by Analyzing Multiple Platform Omics Data from Cr(VI)-Transformed Cells and Their Implications in Lung Cancer

miR-30d-5p: A Non-Coding RNA With Potential Diagnostic, Prognostic and Therapeutic Applications

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