MicroRNA-449b-5p suppresses cell proliferation, migration and invasion by targeting TPD52 in nasopharyngeal carcinoma

Shi, Lei; Mao, Yanjiao

doi:10.1093/jb/mvz057

Cited by 19 publications

(15 citation statements)

References 31 publications

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“…TPD52 was reported as an oncogene in a range of tumors. 21,36,37 In CC, lncRNA HULC silencing reduced TPD52 expression, which inhibited cancer cell invasion and migration. 22 Also, miR-15a-3p reduced the radioresistance of CC cells by targeting TPD52.…”

Section: Discussionmentioning

confidence: 99%

“…Tumor protein D52 (TPD52) is considered to be an oncogene in human cancers, which is isolated from the amplification region of human chromosome 8q21. 19 Previous researches demonstrated that TPD52 acted as an oncogene in lung squamous cell cancer, 20 nasopharyngeal cancer, 21 CC, 22 and prostate cancer. 23 However, the mechanism by which TPD52 participates in CC progression is unclear.…”

Section: Introductionmentioning

confidence: 99%

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<p>Hsa_circ_0084927 Regulates Cervical Cancer Advancement via Regulation of the miR-634/TPD52 Axis</p>

Shi

Zhang

Lou

et al. 2020

CMAR

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Background: Cervical cancer (CC) is a common gynecological tumor that affects women's health. Circular RNA hsa_circ_0084927 (hsa_circ_0084927) has been reported to be upregulated in CC. However, the role and regulatory mechanism of hsa_circ_0084927 in CC are unclear. Methods: Expression of hsa_circ_0084927, microRNA (miR)-634, and tumor protein D52 (TPD52) mRNA in CC tissues and cells was examined by quantitative real-time polymerase chain reaction (qRT-PCR). The proliferation, colony formation, cell cycle progression, apoptosis, migration, and invasion of CC cells were determined with cell counting kit-8 (CCK-8), plate clone, flow cytometry, or transwell assays. The levels of cyclin D1, cleavedcaspase-3 (c-caspase 3), matrix metalloproteinase (MMP)-2, MMP-9, and TPD52 protein were evaluated with Western blotting. The targeting relationship between hsa_circ_0084927 or TPD52 and miR-634 was verified via dual-luciferase reporter and/or RNA immunoprecipitation (RIP) assays. Xenograft assay was conducted to confirm the role of hsa_-circ_0084927 in vivo. Results: Hsa_circ_0084927 and TPD52 were upregulated while miR-634 was downregulated in CC tissues and cells. Hsa_circ_0084927 silencing reduced tumor growth in vivo and induced cell cycle arrest, apoptosis, and curbed proliferation, colony formation, migration, and invasion of CC cells in vitro. Hsa_circ_0084927 regulated TPD52 expression through sponging miR-634. MiR-634 inhibitor reversed hsa_circ_0084927 knockdown-mediated impact on the malignancy of CC cells. TPD52 elevation abolished the repressive influence of miR-634 mimics on the malignancy of CC cells. Conclusion: Hsa_circ_0084927 accelerated CC advancement via upregulating TPD52 via sponging miR-634, offering a new evidence to support hsa_circ_0084927 as a promising target for CC treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

<p>Hsa_circ_0084927 Regulates Cervical Cancer Advancement via Regulation of the miR-634/TPD52 Axis</p>

Shi

Zhang

Lou

et al. 2020

CMAR

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“…However, the pro-apoptosis function of miR-449b-5p was observed in LUAD cells. Previously, extensive studies identified miR-449b-5p as a tumor inhibitor in cancers, including cervical cancer 23 , nasopharyngeal carcinoma 24 , and breast cancer 25,26 . Presently, our work first shed new light on miR-449b-5p function in LUAD together with LINC01123/miR-449b-5p interaction.…”

Section: Discussionmentioning

confidence: 99%

ZEB1-activated LINC01123 accelerates the malignancy in lung adenocarcinoma through NOTCH signaling pathway

et al. 2020

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Growing incidence of lung adenocarcinoma (LUAD) has been detected recently. Multiple long non-coding RNAs (lncRNAs) have been proven as tumor facilitators or inhibitors by extensive works. Present study concentrated on characterizing the potential role of LINC01123 in LUAD. We explored the differential expression of LINC01123 through qRT-PCR and found the amplification of LINC01123 in LUAD cell lines. It was ascertained that LINC01123 was definitely responsible for the malignant processes of LUAD cells. Further, we validated the ceRNA network of LINC01123/miR-449b-5p/NOTCH1 in LUAD via mechanical experiments. As a transcriptional factor related to epithelial mesenchymal transition (EMT), ZEB1 was responsible for the transcriptional activation of both LINC01123 and NOTCH1. The involvement of NOTCH signaling in LUAD was interrogated through evaluating functional changes after treating with FLI-06 (NOTCH pathway suppressor). It showed that FLI-06-caused NOTCH signaling inactivation suppressed malignant functions in LUAD cells. Additionally, LINC01123 facilitated NOTCH1-dependent NOTCH signaling activation. Rescue experiments probed the modulatory function of LINC01123/miR-449b-5p/NOTCH1 in LUAD cellular processes. Altogether, ZEB1-activated LINC01123 accelerates the malignancy in LUAD through miR-449b-5p/NOTCH1 axis-mediated NOTCH signaling pathway, while NOTCH1 boosts ZEB1 in return. These observations suggest the huge potential of LINC01123 as a new target for LUAD therapy.

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“…miRNAs are a family of small non-coding RNAs of approximately 22 nucleotides in length, which regulate gene expression by complementary binding or complex mechanisms (14). In multiple studies, several miRNAs, such as miR-101 (15), miR-184 (16), miR-543 (17) and miR-449 (18), have been demonstrated to suppress proliferation, migration and invasion of NPc. miR-320b was also reported to act as a tumor suppressor during occurrence and progression in different types of cancer, including NPc.…”

Section: Introductionmentioning

confidence: 99%

CircCTDP1 promotes nasopharyngeal carcinoma progression via a microRNA‑320b/HOXA10/TGFβ2 pathway

You

Xue

et al. 2020

Int J Mol Med

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circular RNAs have been reported to play a vital role in the development and progression of various types of cancer. However, the underlying molecular role of circular RNA cTdP1 (circcTdP1) in the tumorigenesis of nasopharyngeal carcinoma (NPc) remains unknown. In the present study, circcTdP1 expression was found to be markedly upregulated in NPc tissues and cell lines (SUNE1, SUNE2 and 6-10B cell lines). Knockdown of circcTdP1 resulted in inhibition of proliferation, migration and invasion, and promoted apoptosis of NPc cells. Moreover, circcTdP1 directly interacted with microRNA (miR)-320b based on bioinformatics prediction and dual luciferase assay, and transfection with an miR-320b inhibitor reversed the effects of circcTdP1 knockdown on NPc cells. Furthermore, circcTdP1/miR-320b promoted NPc progression by regulating the expression of homeobox A10 (HOXA10). In addition, it was demonstrated that HOXA10 may exert its oncogenic role in NPc by regulating the expression of transforming growth factor β2 (TGFβ2). Taken together, these results revealed a novel regulatory mechanism, which may provide an improved understanding of NPc tumorigenesis and be useful in the development of potential targets for NPc therapy.

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MicroRNA-449b-5p suppresses cell proliferation, migration and invasion by targeting TPD52 in nasopharyngeal carcinoma

Cited by 19 publications

References 31 publications

<p>Hsa_circ_0084927 Regulates Cervical Cancer Advancement via Regulation of the miR-634/TPD52 Axis</p>

<p>Hsa_circ_0084927 Regulates Cervical Cancer Advancement via Regulation of the miR-634/TPD52 Axis</p>

ZEB1-activated LINC01123 accelerates the malignancy in lung adenocarcinoma through NOTCH signaling pathway

CircCTDP1 promotes nasopharyngeal carcinoma progression via a microRNA‑320b/HOXA10/TGFβ2 pathway

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