miR‐16‐5p modulates the radiosensitivity of cervical cancer cells via regulating coactivator‐associated arginine methyltransferase 1

Zhang, Shumao; Wang, Weiqing; Wu, Xia; Liu, Weihua

doi:10.1111/pin.12867

Cited by 23 publications

(13 citation statements)

References 36 publications

(43 reference statements)

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“…Then, integrated the above miRs with the upstream miRs of ITGB1, ITGB5, and OSMR predicted by TargetScan website, miR-16 was selected due to it is the common regulator of ITGB1 and ITGB5. Previous researches have indicated that miR-16 was involved in a variety of tumors, including cervical cancer [28], bladder cancer [29], and lung cancer [30]. Our results revealed that miR-16 was significantly decreased in PAAD tissues and patients with low miR-16 expression had poor outcomes.…”

Section: Discussionmentioning

confidence: 52%

Identification of novel candidate biomarkers and efficacious small molecule drugs for pancreatic adenocarcinoma based on comprehensive bioinformatics technology

Yang¹,

Wang²,

Li³

2020

Preprint

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Background: Pancreatic adenocarcinoma (PAAD) is considered as one of most serious solid tumors with high mortality as well as incidence. We performed this present study to screen out novel biomarkers and potential efficacious small drugs in PAAD using integrated bioinformatics analyses. Methods: Expression profiles derived from TCGA and GTEx datasets were integrated by following bioinformatics methods: DEGs analysis, WGCNA, KEGG and GO enrichment analyses. Kaplan-Meier method was conducted to assess the prognostic performance of genes, and the predictive value of identified genes was determined by the ROC analysis. CMap analysis was utilized to identify the related small molecule drugs in PAAD. Results: A total of 4777 DEGs containing 2536 up-regulated and 2241 down-regulated genes were identified. WGCNA identified six modules that were related with clinical characteristics, and functional enrichment analyses showed that all genes of blue module were enriched in EMT, PI3K/Akt signaling pathway and other important biological processes and pathways. Moreover, three genes ( ITGB1 , ITGB5 , and OSMR ) of blue module were determined as key genes with higher expression levels and significant prognostic value. ROC analysis revealed that these three genes had excellent diagnostic efficiency for PAAD. These three key genes were highly regulated in PAAD tissues compared with normal controls. A panel of small molecule drugs including thapsigargin, viomycin, adiphenine, and CP-690334-01 were screened out to treat PAAD. Conclusion: In conclusion, our findings identified three key genes implicated in PAAD and screened out several potential small drugs to treat it, which may shed novel insights into the development of PAAD and its treatment.

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Section: Discussionmentioning

confidence: 52%

Identification of novel candidate biomarkers and efficacious small molecule drugs for pancreatic adenocarcinoma based on comprehensive bioinformatics technology

Yang¹,

Wang²,

Li³

2020

Preprint

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“…For example, lncRNA CR749391 was reported to promote the progression of gastric cancer by sponging miR-181a ( 28 ); lncRNA HCG18 promotes the development of NPC by functioning as a ceRNA of miR-16 to upregulate G1/S-specific cyclin-D1 expression levels ( 29 ) and lncRNA AFAP1-AS1 was observed to function as a ceRNA of miR-423-5p to promote NPC metastasis by activating the Rho/Rac signaling pathway ( 30 ). Previous studies have also indicated that miR-16 is associated with cancer regulation, including cervical cancer, bladder cancer and neuroblastoma ( 31 – 33 ). Consistent with these findings, the present study also observed an interaction between KIF9-AS1 and miR-16 through a series of experiments.…”

Section: Discussionmentioning

confidence: 97%

KIF9‑AS1 promotes nasopharyngeal carcinoma progression by suppressing miR‑16

You

Wang

2020

Oncol Lett

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Long non-coding RNAs (lncRNAs) have been reported to serve a crucial role in the progression of nasopharyngeal carcinoma (NPC); however, the underlying molecular mechanisms of lncRNA KIF9-AS1 in the tumorigenesis of NPC remains poorly understood. Reverse transcription-quantitative PCR was used to analyze the expression levels of KIF9-AS1 and microRNA (miR)-16, and Cell Counting Kit-8, wound healing and Transwell assays were used to determine the cell viability, invasion and migration, respectively, of NPC cells. In addition, a dual-luciferase reporter assay was used to analyze the direct interaction between KIF9-AS1 and miR-16. NPC stage was classified according to the seventh edition of the AJCC staging system. The results revealed that KIF9-AS1 expression levels were upregulated in NPC tissues and cell lines. In addition, miR-16 was demonstrated to directly interact with KIF9-AS1 and inhibit KIF9-AS1 expression levels, whereas the miR-16 inhibitor rescued the effects of the KIF9-AS1-knockdown in NPC cells. Furthermore, the expression levels of KIF9-AS1 were upregulated, while those of miR-16 were downregulated in NPC tissues. Notably, the expression levels of KIF9-AS1 were observed to be significantly more upregulated in advanced tumors (III–IV vs. I–II) and patients with high KIF9-AS1 expression levels exhibited a worse prognosis. In conclusion, the findings of the present study suggested that KIF9-AS1 may promote the progression of NPC by targeting miR-16, thus KIF9-AS1 may be a novel molecular target for NPC therapy.

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“…In this study, LINC00662 was validated to bind to miR-16-5p. Previous investigations have shown that miR-16-5p is differentially expressed and plays a key role in the progression of numerous cancers, such as breast cancer [ 29 ], cervical cancer [ 30 ], and hepatocellular carcinoma [ 31 ]. In the present study, miR-16-5p was expressed at a low level in OS tissues and cells and negatively related to LINC00662 in terms of expression level.…”

Section: Discussionmentioning

confidence: 99%

LncRNA LINC00662 Exerts an Oncogenic Effect on Osteosarcoma by the miR-16-5p/ITPR1 Axis

Cao

et al. 2021

Journal of Oncology

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Background. Osteosarcoma (OS) is one of the most malignant bone tumors and has a high metastatic rate. Increasing research has demonstrated the vital roles of long noncoding RNAs (lncRNAs) in human cancers, including OS. LncRNA LINC00662 has been revealed to act as an oncogene involved in multiple tumor progression. This study aimed to investigate the expression pattern, function, and regulatory mechanism of LINC00662 in OS. Methods. Patients who underwent OS surgery were involved in this study. Experiments including RT-qPCR, MTT, western blot, FISH, RNA pull-down, luciferase reporter, colony formation, transwell invasion and migration, and sphere formation assay were performed to investigate the regulatory role of LINC00662 in OS. Results. In the present study, our findings demonstrated the upregulation of LINC00662 expression in OS tissues and cells, and high expression of LINC00662 predicted a poor clinical prognosis of patients’ iNOS. Through a series of in vivo assays, LINC00662 knockdown suppressed OS cell proliferation, invasion, migration, and stemness property maintenance. Further mechanistical investigations indicated that LINC00662 functioned as a competing endogenous RNA (ceRNA) for sponging microRNA-16-5p (miR-16-5p) to upregulate the expression of IP receptor type 1 (ITPR1) in OS cells. Restoration assays validated the involvement of ITPR1 in LINC00662-mediated regulation of cell functions in OS. Conclusion. LINC00662 exerts oncogenic functions in OS by targeting the miR-16-5p/ITPR1 axis.

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miR‐16‐5p modulates the radiosensitivity of cervical cancer cells via regulating coactivator‐associated arginine methyltransferase 1

Cited by 23 publications

References 36 publications

Identification of novel candidate biomarkers and efficacious small molecule drugs for pancreatic adenocarcinoma based on comprehensive bioinformatics technology

Identification of novel candidate biomarkers and efficacious small molecule drugs for pancreatic adenocarcinoma based on comprehensive bioinformatics technology

KIF9‑AS1 promotes nasopharyngeal carcinoma progression by suppressing miR‑16

LncRNA LINC00662 Exerts an Oncogenic Effect on Osteosarcoma by the miR-16-5p/ITPR1 Axis

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