miRNA-425-5p enhances lung cancer growth via the PTEN/PI3K/AKT signaling axis

Zhou, Jinshan; Yang, Ze-shan; Cheng, Siyang; Yu, Jianghao; Huang, Chengming; Feng, Qiang

doi:10.1186/s12890-020-01261-0

Cited by 28 publications

(17 citation statements)

References 24 publications

(26 reference statements)

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“…miRNAs are non-coding RNAs of approximately 20 nucleotides, which typically function by degrading the expression of their target genes [ 15 ]. Dysregulation of miRNAs has been regarded as a critical factor in cancer cell growth and apoptosis in cancers such as colon, ovarian, and lung cancer [ 16 – 18 ]. Both miR-490-3p and miR-490-5p are members of the miR-490 family, which participate in tumorigenesis [ 19 , 20 ].…”

Section: Introductionmentioning

confidence: 99%

LINC00958 promotes bladder cancer carcinogenesis by targeting miR-490-3p and AURKA

Zhen

et al. 2021

BMC Cancer

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Background Bladder cancer is a prevalent malignancy of the urinary system, in which long non-coding RNAs (lncRNAs) are highly associated. We aimed to elucidate the role of LINC00958 in bladder cancer. Methods LINC00958 expression levels were measured using qRT-PCR. The interaction of LINC00958-miR-490-3p-AURKA was analyzed by luciferase, RIP, and RNA pull-down assays. The biological roles of LINC00958, miR-490-3p, and AURKA in bladder cancer cells were analyzed using CCK8, BrdU, and transwell assays. Results Increased expression of LINC00958 and AURKA was observed in bladder cancer tissues and cell lines. Decreased LINC00958 expression repressed bladder cancer progression and downregulation of miR-490-3p accelerated bladder cancer cell progression. Moreover, LINC00958 sponges miR-490-3p to upregulate AURKA expression, thereby promoting carcinogenesis in bladder cancer cells. Conclusions Our study revealed that LINC00958 facilitated cell proliferation and invasion, and suppressed cell apoptosis by sponging miR-490-3p and upregulating AURKA, thus inspiring a new treatment method for bladder cancer.

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Section: Introductionmentioning

confidence: 99%

LINC00958 promotes bladder cancer carcinogenesis by targeting miR-490-3p and AURKA

Zhen

et al. 2021

BMC Cancer

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“…MiRNAs have been confirmed to participate in post-transcriptional gene expression regulation, acting as oncogenes or tumor suppressors [ 30 , 31 ]. In addition, the evidence demonstrated that tumor cells exhibit increased intrinsic ROS stress due to increased metabolic activity and mitochondrial malfunction [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

Acidic Tumor Microenvironment Promotes Pancreatic Cancer through miR-451a/MEF2D Axis

Yao

et al. 2022

Journal of Oncology

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Pancreatic cancer (PC), as a highly malignant and aggressive solid tumor, is common in the digestive system. The acidic microenvironment is one of the critical markers of cancer. Nonetheless, there are few studies on how the acidic microenvironment affects the development of PC. This study focused on investigating the specific molecular mechanisms of the acidic microenvironment in PC. In our study, qRT-PCR was conducted for examining microRNA (miR)-451a and myocyte enhancer factor 2D (MEF2D) expressions in PANC-1 cells. Then, detailed functional effects of an acidic environment on miR-451a and MEF2D in PANC-1 cells were detected by CCK-8, colony formation, flow cytometry, wound healing, transwell, mitochondrial functionality measurement, JC-1 staining, DCFH-DA staining, and sphere formation assays. The relationship between miR-451a and MEF2D was confirmed by luciferase reporter analysis. Under acidic conditions, the increase of proliferation, migration, and invasion of PANC-1 cells was observed. Moreover, the mitochondrial oxidative respiration-related gene miR-451a was reduced in acidic conditions. In addition, we found that, in PANC-1 cells under an acidic environment, miR-451a overexpression enhanced oxygen consumption, mitochondrial membrane potential (MMP) loss, and ROS generation and inhibited proliferation, migration, invasion, and stemness via sponging MEF2D. In a word, our results revealed that the acidic microenvironment regulated PC progression by affecting the miR-451a/MEF2D axis, indicating a novel avenue for the future treatment of PC.

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“…In breast cancer, miR-425-5p promotes cell growth by target binding to the PTEN 3‘UTR [ 21 ]. In lung cancer, miR-425-5p overexpression is positively associated with poor prognosis and enhances the proliferation, migration, and invasion of cells [ 22 , 23 ]. In renal cell carcinoma, studies have shown that miR-425-5p is an oncogene in this cancer [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

MiR-425-5p accelerated the proliferation, migration, and invasion of ovarian cancer cells via targeting AFF4

Guo

Zhang³

et al. 2021

J Ovarian Res

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Background Accumulating data have established that microRNAs (miRNAs) play significant regulatory roles in the carcinogenesis and progression of ovarian cancer (OC). MiR-425-5p was reported to function in various tumors. However, the roles and underlying mechanism of miR-425-5p involvement in OC development and progression are unclear. Methods A comprehensive strategy of data mining, computational biology, and real-time polymerase chain reaction was employed to identify the involvement of miR-425-5p in OC progression. The effect of miR-425-5p on the proliferation, migration, and invasion of OC cells was determined using Cell Counting Kit-8, wound-healing, and Matrigel invasion assays, respectively. Luciferase assay was performed to evaluate the interactions between miR-425-5p and MAGI2-AS3 or AFF4. Results miR-425-5p was significantly up-regulated in OC tissues and cells. The luciferase reporter assay revealed that miR-425-5p was negatively regulated by MAGI2-AS3. Silencing miR-425-5p inhibited the proliferation, migration, and invasion of OC cells in vitro. Bioinformatics analysis and luciferase reporter assay revealed that AFF4 was the target gene of miR-425-5p. Moreover, AFF4 expression was significantly decreased in OC and was closely related to the good prognosis of patients with OC. AFF4 overexpression inhibited the proliferation, migration, and invasion of OC cells in vitro. By contrast, silencing AFF4 promoted the proliferation, migration, and invasion of OC cells in vitro. Finally, AFF4 suppression rescued the inhibitory effect of silencing miR-425-5p on the proliferation, migration, and invasion of OC cells. Conclusion To the best our knowledge, this is the first study to demonstrate that miR-425-5p overexpression in OC is negatively regulated by MAGI2-AS3. Moreover, miR-425-5p promotes the proliferation, migration, and invasion of OC cells by targeting AFF4, suggesting that miR-425-5p/AFF4 signaling pathway represented a novel therapeutic target for patients with OC.

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miRNA-425-5p enhances lung cancer growth via the PTEN/PI3K/AKT signaling axis

Cited by 28 publications

References 24 publications

LINC00958 promotes bladder cancer carcinogenesis by targeting miR-490-3p and AURKA

LINC00958 promotes bladder cancer carcinogenesis by targeting miR-490-3p and AURKA

Acidic Tumor Microenvironment Promotes Pancreatic Cancer through miR-451a/MEF2D Axis

MiR-425-5p accelerated the proliferation, migration, and invasion of ovarian cancer cells via targeting AFF4

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