MicroRNA‑342‑3p functions as a tumor suppressor by targeting LIM and SH3 protein 1 in oral squamous cell carcinoma

Song, Xian‐Rong; Jin, Yong; Yan, Min; Zhang, Yonggang; Chen, Bing

doi:10.3892/ol.2018.9637

Cited by 8 publications

(9 citation statements)

References 37 publications

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“… 18 MiR-342-3p functions as a tumor suppressor in oral squamous cell carcinoma (OSCC) by targeting LIM and SH3 protein 1 ( LASP1 ) and may act as a promising therapeutic target for OSCC. 19 In the present study, we found that miR-342-3p was downregulated in NSCLC tissues and cells, indicating that it may be a tumor suppressor in NSCLC, which is consistent with the above findings.…”

Section: Discussionsupporting

confidence: 92%

miR-342-3p Regulates the Proliferation and Apoptosis of NSCLC Cells by Targeting BCL-2

Chen

Ying

Shang

et al. 2021

Technol Cancer Res Treat

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microRNA-342-3p plays an important role in tumor occurrence and development. However, the expression pattern and roles of microRNA-342-3p in nonsmall cell lung cancer remain poorly understood. In the current study, we explored the roles and underlying mechanisms of microRNA-342-3p in nonsmall cell lung cancer via gain- and loss-of-function analyses. We used quantitative reverse-transcription-polymerase chain reaction and western blotting assays to measure the expression levels of microRNA-342-3p in nonsmall-cell lung cancer and B-cell lymphoma-2. Furthermore, we used small interfering RNA and RNA mimics to analyze the functions and underlying mechanisms of microRNA-342-3p in nonsmall cell lung cancer cells. A luciferase reporter assay was performed to evaluate the direct binding site of the 5′-untranslated region of B-cell lymphoma-2 targeted by microRNA-342-3p. We found that the expression of microRNA-342-3p was significantly lower in nonsmall cell lung cancer cells and tissues than in normal cells and tissues. The upregulation of microRNA-342-3p suppressed cell proliferation while promoting apoptosis in H1975, H460, and H226 cells. The overexpression of microRNA-342-3p in nonsmall cell lung cancer cells led to the downregulation of mRNA and protein levels in B-cell lymphoma-2 cells. Thus, B-cell lymphoma-2 was identified as a direct target of microRNA-342-3p. These findings indicate that microRNA-342-3p inhibits the growth of nonsmall cell lung cancer by repressing the expression of B-cell lymphoma-2, which suggests that microRNA-342-3p could be a potential target for the treatment of nonsmall cell lung cancer.

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Section: Discussionsupporting

confidence: 92%

miR-342-3p Regulates the Proliferation and Apoptosis of NSCLC Cells by Targeting BCL-2

Chen

Ying

Shang

et al. 2021

Technol Cancer Res Treat

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“…LASP1 is highly expressed in different kinds of tumors as an adhesive protein, and in U87 and LN229 glioma cells . The LASP1 gene promotes the proliferation of oral squamous cell carcinoma cells . It is also highly expressed in breast cancer tissues and cells, and downregulation of LASP1 inhibits proliferation, migration, and invasion of breast cancer cells .…”

Section: Discussionmentioning

confidence: 99%

“…37 The LASP1 gene promotes the proliferation of oral squamous cell carcinoma cells. 38 It is also highly expressed in breast cancer tissues and cells, and downregulation of LASP1 inhibits proliferation, migration, and invasion of breast cancer cells. 39 LASP1 functions as an oncogene in liver cancer and promotes the occurrence and development of hepatoma cells.…”

Section: Discussionmentioning

confidence: 99%

Transcription factor AP‐4 (TFAP4)‐upstream ORF coding 66 aa inhibits the malignant behaviors of glioma cells by suppressing the TFAP4/long noncoding RNA 00520/microRNA‐520f‐3p feedback loop

et al. 2020

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Upstream ORF (uORF) is a translational initiation element located in the 5′UTR of eukaryotic mRNAs. Studies have found that uORFs play an important regulatory role in many diseases. Based on The Cancer Genome Atlas database, the results of our experiments and previous research evidence, we investigated transcription factor AP‐4 (TFAP4) and its uORF, LIM and SH3 protein 1 (LASP1), long noncoding RNA 00520 (LINC00520), and microRNA (miR)‐520f‐3p as candidates involved in glioma malignancy, which is a poorly understood process. Both TFAP4‐66aa‐uORF and miR‐520f‐3p were downregulated, and TFAP4, LASP1, and LINC00520 were highly expressed in glioma tissues and cells. TFAP4‐66aa‐uORF or miR‐520f‐3p overexpression or TFAP4, LASP1, or LINC00520 knockdown inhibited glioma cell proliferation, migration, and invasion, but promoted apoptosis. TFAP4‐66aa‐uORF inhibited the translation of TFAP4 by binding to the TFAP4 mRNA. MicroRNA‐520f‐3p inhibited TFAP4 expression by binding to its 3′UTR. However, LINC00520 could promote the expression of TFAP4 by competitively binding to miR‐520f‐3p. In addition, TFAP4 transcriptionally activated LASP1 and LINC00520 expression by binding to their promoter regions, forming a positive feedback loop of TFAP4/LINC00520/miR‐520f‐3p. Our findings together indicated that TFAP4‐66aa‐uORF inhibited the TFAP4/LINC00520/miR‐520f‐3p feedback loop by directly inhibiting TFAP4 expression, subsequently leading to inhibition of glioma malignancy. This provides a basis for developing new therapeutic approaches for glioma treatment.

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“…MiR-152-5p functions as an upstream gene of FOXO to restrain cell proliferation and boost cell apoptosis in liver cancer [30]. It has been identified that miR-342-3p act as a tumor suppressor in oral squamous cell carcinoma [31], gastric cancer [32], hepatocellular carcinoma [33] and so on. However, its role in CC has not been elucidated.…”

Section: Discussionmentioning

confidence: 99%

LncRNA LINC01503 aggravates the progression of cervical cancer through sponging miR-342-3p to mediate FXYD3 expression

et al. 2020

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Cervical cancer (CC), an aggressive malignancy, has a high risk of relapse and death, mainly occurring in females. Accumulating investigations have confirmed the critical role of long noncoding RNAs (lncRNAs) in diverse cancers. LncRNA LINC01503 has been reported as an oncogene in several cancers. Nonetheless, its role and molecular mechanism in CC have not been explored. In the present study, we found that FXYD3 expression was considerably up-regulated in CC tissues and cells. Moreover, FXYD3 deficiency conspicuously hampered cell proliferation and migration while facilitated cell apoptosis in CC cells. Subsequently, molecular mechanism experiments implied that FXYD3 was a downstream target gene of miR-342-3p, and FXYD3 expression was reversely mediated by miR-342-3p. Moreover, we discovered that LINC01503 acted as the endogenous sponge for miR-342-3p. Besides, LINC01503 negatively regulated miR-342-3p expression and positively regulated FXYD3 expression in CC. Rescue assays revealed that LINC01503 depletion-induced repression on CC progression could be partly recovered by miR-342-3p inhibition, and then the co-transfection of sh-FXYD3#1 rescued this effect. Conclusively, LINC01503 aggravated CC progression through sponging miR-342-3p to mediate FXYD3 expression, providing promising therapeutic targets for CC patients.

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MicroRNA‑342‑3p functions as a tumor suppressor by targeting LIM and SH3 protein 1 in oral squamous cell carcinoma

Cited by 8 publications

References 37 publications

miR-342-3p Regulates the Proliferation and Apoptosis of NSCLC Cells by Targeting BCL-2

miR-342-3p Regulates the Proliferation and Apoptosis of NSCLC Cells by Targeting BCL-2

Transcription factor AP‐4 (TFAP4)‐upstream ORF coding 66 aa inhibits the malignant behaviors of glioma cells by suppressing the TFAP4/long noncoding RNA 00520/microRNA‐520f‐3p feedback loop

LncRNA LINC01503 aggravates the progression of cervical cancer through sponging miR-342-3p to mediate FXYD3 expression

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