<scp>miR</scp>‐744‐5p inhibits cellular proliferation and invasion via targeting <scp>ARF1</scp> in epithelial ovarian cancer

Zhao, Lai-Gang; Wang, Jiao; Jin, Li; Li, Qinfen

doi:10.1002/kjm2.12253

Cited by 19 publications

(14 citation statements)

References 26 publications

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“…Furthermore, MiR-744-5p has been shown to slow the progression of OC [ 21 , 29 ]. Therefore, we speculated that MNX1-AS1 regulates the OC process through sponging to miR-744-5p.…”

Section: Discussionmentioning

confidence: 99%

LncRNA MNX1-AS1 promotes ovarian cancer process via targeting the miR-744-5p/SOX12 axis

Shen

Fang

et al. 2021

J Ovarian Res

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Purpose Ovarian cancer (OC) is the most common malignancy in women with high mortality. Increasing studies have revealed that long non-coding RNA (lncRNA) MNX1-AS1 has a promoting effect on various cancers. However, the mechanisms of MNX1-AS1 in OC are still unclear. Therefore, this study focused on exploring the mechanisms of MNX1-AS1 in OC. Materials and methods The expression of SOX12 at the protein level was detected by western blot. Cell proliferation was detected by CCK8 assay and colony formation assay. Cell cycle and cell apoptosis were detected by flow cytometry. Wound-healing assay, transwell assay and western blot were used to detect the ability of cell migration and invasion. The target binding was confirmed through the luciferase reporter assay. Results The expression of MNX1-AS1 was increased in OC tumor tissues and cells. Elevated MNX1-AS1 expression is associated with advanced stage and lower overall survival rate. Knockdown of MNX1-AS1 inhibited cell proliferation, migration and invasion, blocked cell cycle, and promoted cell apoptosis in SKOV-3 and OVCAR-3 cells. MNX1-AS1 was competitively binding with miR-744-5p, and its downstream target gene was SOX12. miR-544-5p expression was decreased, while SOX12 expression was increased in OC tumor tissues and cells. Overexpression of miR-744-5p inhibited cell proliferation, migration, invasion and promoted cell apoptosis in SKOV-3 and OVCAR-3 cells. Conclusion MNX1-AS1 promoted the development of OC through miR-744-5p/SOX12 axis. This study revealed a novel mechanism of MNX1-AS1 in OC, which may provide a new treatment or scanning target for OC.

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“…Furthermore, MiR-744-5p has been shown to slow the progression of OC [ 21 , 29 ]. Therefore, we speculated that MNX1-AS1 regulates the OC process through sponging to miR-744-5p.…”

Section: Discussionmentioning

confidence: 99%

LncRNA MNX1-AS1 promotes ovarian cancer process via targeting the miR-744-5p/SOX12 axis

Shen

Fang

et al. 2021

J Ovarian Res

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“…Previous studies have revealed that the expression levels of miR-744-5p were associated with the occurrence and development of multiple types of cancer ( 4 , 27 ). For instance, the upregulated expression of miR-744-5p inhibited the proliferation and migration of ovarian cancer cells ( 28 ), and higher levels of miR-744-5p also repressed the proliferation and invasion of lung cancer cells by regulating the expression of paired box 2 ( 13 ). However, the present study reported that the lncRNA HOTTIP targeted and negatively regulated miR-744-5p, and the knockdown of miR-744-5p partially reversed the HOTTIP-induced inhibitory effect on the proliferation and migration of A549 cells.…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA HOTTIP enhances the fibrosis of lung tissues by regulating the miR‑744‑5p/PTBP1 signaling axis

Chai

Zhao

et al. 2021

Mol Med Rep

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Fibrosis of lung tissue can induce the occurrence and development of numerous types of lung disease. The expression levels of the long non-coding RNA (lncRNA) HOXA distal transcript antisense RNA (HOTTIP) have been reported to be upregulated during the development of fibrosis in liver tissues, which subsequently activated hepatic stellate cells. However, whether the lncRNA HOTTIP participates in the occurrence and development of lung fibrosis remains unknown. The present study aimed to investigate the role of lncRNA HOTTIP in lung fibrosis and its potential mechanism. In the present study, A549 cells were stimulated with TGF-β1 to induce lung fibrosis in vitro. A549 was transfected with short hairpin RNA-HOTTP, overexpression-polypyrimidine tract binding protein 1 (PTBP1), microRNA (miR)-744-5p mimic or miR-744-5p to regulate gene expression. Cell proliferation and migration were determined using 5'-ethynl-2'-deoxyuridine and wound healing assays, respectively. The expression levels of α-smooth muscle actin, collagen I, collagen III and fibronectin 1 were analyzed using western blotting. starBase was used to identify molecules that may interact with the lncRNA HOTTIP and dual luciferase reporter assays were used to validate the findings. Moreover, an in vivo lung fibrosis model was established by bleomycin induction in mice. Histological injury was observed using hematoxylin and eosin and masson staining. The results of the present study revealed that the proliferation and migration of A549 cells were both suppressed following the knockdown of HOTTIP. The lncRNA HOTTIP was found to target and downregulate the expression levels of miR-744-5p. The overexpression of miR-744-5p inhibited the proliferation and migration of A549 cells. Furthermore, miR-744-5p targeted and downregulated the expression levels of PTBP1. It was subsequently demonstrated that the overexpression of PTBP1 rescued miR-744-5p-induced suppression of the proliferation and migration of A549 cells. The knockdown of lncRNA HOTTIP expression also relieved the fibrosis of the lung tissues of mice. In conclusion, the results of the present study suggested that the lncRNA HOTTIP may promote the fibrosis of lung tissues by downregulating the expression levels of miR-744-5p and upregulating the expression levels of PTBP1.

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“…On the contrary, miR-652 is reported to promote tumorigenesis and metastasis through targeting RORA [41]. miR-744-5p has been reported to play a negatively regulatory role in some cancers like ovarian cancer and non-small cell lung cancer, however, few studies investigate the effects and mechanism of miR-744-5p in OS [17][18][19]. In accordance with the data from GEO database and results of qRT-PCR, we found that miR-744-5p was down-regulated in the OS cells and tissue samples, which was consistent with previous studies.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, partial miRNAs participate in the course of EMT and act on the regulation of tumors [15,16]. miR-744-5p has been reported to be up-regulated in several tumors and was closely related with the clinical characteristics [17][18][19][20]. However, the functions of miR-744-5p in OS has not been reported and the mechanism of action of miR-744-5p still needs further study.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-744-5p Suppresses Tumorigenesis and Metastasis of Osteosarcoma Through the MAPK/ERK Signaling Pathway by Targeting TGFB1

Liang

Tan

et al. 2021

Preprint

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Background: Osteosarcoma (OS) is the most common malignant bone tumor in children and adolescents, and accumulating evidence has revealed that microRNAs (miRNAs) exert a crucial part in the progression of OS. Methods: GSE65071 from the GEO database was analyzed and miR-744-5p was found to be the lowest expressed miRNA. Real-time quantitative PCR (qRT-PCR), Western blotting (WB), colony formation assay, 5-Ethynyl-2-Deoxyuridine (EdU) incorporation assay and Transwell migration and invasion assay were performed to examine the effects of miR-744-5p in vitro, Luciferase-reporter assay was performed to detect the interactions between miR-744-5p and its specific target gene. Subcutaneous tumor-forming animal models and tail vein injection lung metastatic models were conducted in animal experiments to detect the effects of miR-744-5p in vivo. Results: miR-744-5p expression was down-regulated in OS cells and tissues. Higher expression of miR-744-5p was related with better clinical prognosis and lower malignancy degree of OS, including cell proliferation, migration and invasion in vitro and vivo. Transforming growth factor-β1 (TGFB1) was negatively regulated by miR-744-5p and could reverse the effects of miR-744-5p on OS proliferation, migration and invasion. The MAPK/ERK signaling pathway was involved in the miR-744-5p/TGFB1 axis. Conclusions: In general, this study suggests that miR-744-5p is a negative regulator of TGFB1, and suppresses OS progression and metastasis via MAPK/ERK signaling pathway.

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miR‐744‐5p inhibits cellular proliferation and invasion via targeting ARF1 in epithelial ovarian cancer

Cited by 19 publications

References 26 publications

LncRNA MNX1-AS1 promotes ovarian cancer process via targeting the miR-744-5p/SOX12 axis

LncRNA MNX1-AS1 promotes ovarian cancer process via targeting the miR-744-5p/SOX12 axis

Long non‑coding RNA HOTTIP enhances the fibrosis of lung tissues by regulating the miR‑744‑5p/PTBP1 signaling axis

MicroRNA-744-5p Suppresses Tumorigenesis and Metastasis of Osteosarcoma Through the MAPK/ERK Signaling Pathway by Targeting TGFB1

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