&lt;p&gt;LncRNA PART1 Exerts Tumor-Suppressive Functions in Tongue Squamous Cell Carcinoma via miR-503-5p&lt;/p&gt;

Zhao, Xiqun; Yanqing, Hong; Cheng, Qingyuan; Guo, Lixin

doi:10.2147/ott.s264410

Cited by 20 publications

(13 citation statements)

References 39 publications

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“…An increasing number of studies have focused on the expression status and specific roles of lncRNAs in TSCC. For instance, PART1, 26 FALEC, 27 and LINC00961 28 were weakly expressed in TSCC and performed antioncogenic roles. In contrast, UCA1, 29 PHACTR2-AS1, 30 and FOXD2-AS1 31 were expressed at high levels in TSCC and performed pro-oncogenic actions during TSCC progression.…”

Section: Discussionmentioning

confidence: 99%

LncRNA NOP14-AS1 Promotes Tongue Squamous Cell Carcinoma Progression by Targeting MicroRNA-665/HMGB3 Axis

Li¹,

Fan²,

Liu³

et al. 2021

CMAR

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Purpose The expression profile, clinical effects, and detailed roles of NOP14 antisense RNA 1 (NOP14-AS1) in tongue squamous cell carcinoma (TSCC) remain ambiguous and need to be further explored. Thus, this work was initiated to offer further solid evidence regarding the expression and roles of NOP14-AS1 in TSCC. Furthermore, additional efforts were exerted to reveal the molecular events by which NOP14-AS1 affects the malignant behaviours of TSCC. Methods NOP14-AS1 expression was detected in TSCC tissues and cell lines using quantitative reverse transcription-polymerase chain reaction. Cell Counting Kit-8 assay, flow cytometric analysis, Transwell migration and invasion assays, and xenograft tumor model analysis were performed to assess the malignant biological behaviors of TSCC cells after NOP14-AS1 depletion. Mechanistic studies were performed using bioinformatics analysis, luciferase reporter assay, RNA immunoprecipitation, and rescue experiments. Results NOP14-AS1 upregulation was identified in TSCC tissues and cell lines. Patients with TSCC exhibiting a high NOP14-AS1 expression faced shorter overall survival than those with a low NOP14-AS1 expression. Functionally, NOP14-AS1 depletion facilitated apoptosis and impeded cell proliferation, migration, and invasion in TSCC. In vivo, the growth of TSCC cells was hindered by NOP14-AS1 depletion. Mechanically, NOP14-AS1 functioned as a competing endogenous RNA by sponging microRNA-665 (miR-665), thereby overexpressing the target high mobility group box 3 (HMGB3) of miR-665. Lastly, rescue experiments confirmed that the introduction of HMGB3 overexpression plasmid or miR-665 inhibitor could abrogate the inhibition of aggressive phenotypes triggered by NOP14-AS1 knockdown. Conclusion NOP14-AS1 executed pro-oncogenic activities in TSCC cells by targeting the miR-665/HMGB3 axis. The NOP14-AS1/miR-665/HMGB pathway may be a valuable prognostic indicator and therapeutic target for preventing TSCC.

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Section: Discussionmentioning

confidence: 99%

LncRNA NOP14-AS1 Promotes Tongue Squamous Cell Carcinoma Progression by Targeting MicroRNA-665/HMGB3 Axis

Li¹,

Fan²,

Liu³

et al. 2021

CMAR

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“…Previous reference showed that CASC9 induced TSCC cell growth, invasion and migration via modulating miR‐423‐5p/SOX12 34 . PART1 inhibited TSCC cell growth, migration and invasion through regulating miR‐503‐5p 35 . Another study indicated that lncRNA ELDR increased cell growth through inducing cyclin E1‐ILF3 signalling in oral tumour 36 .…”

Section: Discussionmentioning

confidence: 96%

LINC01783 accelerated tongue squamous cell carcinoma progression via inhibiting miR‐199b‐5p

Wang

et al. 2021

J Cellular Molecular Medi

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Growing studies illustrated that lncRNAs exert critical roles in development and occurrence of tumours including TSCC. In this research, we indicated that LINC01783 was up‐regulated in TSCC cells (SCC1, Cal27, UM1 and SCC4) when compared to NHOK cell. RT‐qPCR analysis indicated that LINC01783 was overexpressed in 22 TSCC cases (73.3%, 22/30) compared with no‐tumour specimens. LINC01783 level was up‐regulated in TSCC specimens when compared to no‐tumour specimens. Ectopic expression of LINC01783 promoted TSCC cell cycle and growth and EMT progression in both TSCC cell SCC1 and Cal27. Overexpression of LINC01783 sponged miR‐199b‐5p in TSCC cell and elevated expression of LINC01783 inhibited miR‐199b‐5p expression. Moreover, we illustrated that miR‐199b‐5p was down‐regulated in TSCC cells and specimen and LINC01783 level was up‐regulated in TSCC specimens when compared to no‐tumour specimens. Elevated expression of LINC01783 promoted TSCC cell growth, cycle and EMT progression by sponging miR‐199b‐5p. These data suggested that LINC01783 functioned as one oncogene and might be one treatment target for TSCC.

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“…Additionally, decreased miR-503 can enhance the drug resistance of OC [ 19 ], and is strongly associated with the increasing rate of cell proliferation and metastasis in OC [ 20 ]. It is acknowledged that lncRNAs can act as competing endogenous RNAs or sponges of miRNAs in cancer progression [ 21 , 22 ]. Sun et al have confirmed that MALAT1 can interact with miR-503-5p to mediate OC cell proliferation and apoptosis [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

“…Sun et al have confirmed that MALAT1 can interact with miR-503-5p to mediate OC cell proliferation and apoptosis [ 21 ]. PART1 may act as a competing endogenous RNA of miR-503-5p in tongue squamous cell carcinoma to modulate cancer progression [ 22 ]. PART1 also accelerates cisplatin (DDP) resistance of OC via regulation of miR-512-3p, suggesting PART1 may be a promising therapeutic target for DDP-resistant OC patients [ 23 ].…”

Section: Introductionmentioning

confidence: 99%

Repression of lncRNA PART1 attenuates ovarian cancer cell viability, migration and invasion through the miR-503-5p/FOXK1 axis

Li¹,

Lou²,

Zhang³

et al. 2022

BMC Cancer

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Background Ovarian cancer (OC) is a female malignant tumor with a high fatality rate. Long non-coding RNAs (lncRNAs) are deeply involved in OC progression. The aim of this study is to explore the specific mechanism of lncRNA prostate androgen-regulated transcript 1 (PART1) in OC. Methods Quantitative real time PCR was utilized to determine the expression levels of PART1, microRNA (miR)-503-5p and forkhead-box k1 (FOXK1) in OC tissues and/or cells. The cell viability, migration, and invasion in OC were evaluated by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-h-tetrazolium bromide assay, wound healing assay and transwell invasion assay, respectively. Flow cytometry was used to analyze the cell apoptosis. The xenograft tumor was conducted in nude mice to verify the effect of PART1 knockdown on OC in vivo. The target relationships among PART1, miR-503-5p and FOXK1 were predicted by StarBase, and verified by luciferase reporter assay. The level of FOXK1 was assessed by western blot. Results Increased expression of PART1 and FOXK1 was observed in OC tissues or cells, whereas miR-503-5p was downregulated. PART1 silencing or miR-503-5p overexpression repressed the cell viability, migration and invasion, and protomed apoptosis. Meanwhile, miR-503-5p was a target of PART1, and FOXK1 was a direct target gene of miR-503-5p. Both downregulation of miR-503-5p and upregulation of FOXK1 partly relieved the suppressive effects of PART1 knockdown on the oncogenicity of OC in vitro. Conclusion Decreased PART1 represses the cell viability, migration and invasion of OC via regulating the miR-503-5p/FOXK1 axis, which provided an underlying target for treating OC.

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<p>LncRNA PART1 Exerts Tumor-Suppressive Functions in Tongue Squamous Cell Carcinoma via miR-503-5p</p>

Cited by 20 publications

References 39 publications

LncRNA NOP14-AS1 Promotes Tongue Squamous Cell Carcinoma Progression by Targeting MicroRNA-665/HMGB3 Axis

LncRNA NOP14-AS1 Promotes Tongue Squamous Cell Carcinoma Progression by Targeting MicroRNA-665/HMGB3 Axis

LINC01783 accelerated tongue squamous cell carcinoma progression via inhibiting miR‐199b‐5p

Repression of lncRNA PART1 attenuates ovarian cancer cell viability, migration and invasion through the miR-503-5p/FOXK1 axis

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