Altered expression of lncRNA NCK1‑AS1 distinguished patients with prostate cancer from those with benign prostatic hyperplasia

Guan, Zhihui; Song, Yuwei; Ma, Jinguo; Li, Feng; Zhao, Xiaojun; Liang, Guodong; An, Haiquan; Pu, Jinxian

doi:10.3892/ol.2019.11039

Cited by 7 publications

(10 citation statements)

References 26 publications

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“…Besides, NCK1-AS1 has been validated to accelerate the development of ovarian cancer [ 19 ]. In addition, its promoting role in prostate cancer [ 11 ], osteosarcoma [ 12 ], cervical cancer [ 13 ], glioma [ 14 ], etc. gives more evidence to the research value of the investigation into NCK1-AS1 in human cancers.…”

Section: Discussionmentioning

confidence: 99%

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NCK1-AS1 promotes the progression of melanoma by accelerating cell proliferation and migration via targeting miR-526b-5p/ADAM15 axis

et al. 2021

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Background Long non-coding RNAs (lncRNAs) are vital regulators of gene expression and cellular processes in multiple cancers, including melanoma. Nevertheless, the function of lncRNA NCK1-antisense 1 (NCK1-AS1) in melanoma remains unknown. Methods RT-qPCR was used to analyze the expression of NCK1-AS1, microRNA-526b-5p (miR-526b-5p) and ADAM metallopeptidase domain 15 (ADAM15). Cell proliferation was determined by CCK-8, colony formation and EdU assays. Cell migration was assessed by transwell migration and wound healing assays. Mechanism experiments including luciferase reporter, RIP and RNA pull down assays were conducted to demonstrate the interactions between RNAs. Xenograft model was established to verify the function of NCK1-AS1 and miR-526b-5p in melanoma in vivo. Results NCK1-AS1 was overexpressed in melanoma cell lines and NCK1-AS1 knockdown hampers the proliferation and migration of melanoma cells. Besides, miR-526b-5p binds to NCK1-AS1 in melanoma and ADAM15 was validated as its downstream target. Further, the inhibitory effects of NCK1-AS1 knockdown on cell proliferation and migration in melanoma were reversed by the depletion of miR-526b-5p and further counteracted by ADAM15 knockdown. The growth of melanoma tumors was hindered by the down-regulation of NCK1-AS1 or up-regulation of miR-526b-5p. Conclusion NCK1-AS1 facilitates cell proliferation and migration in melanoma via targeting miR-526b-5p/ADAM15 axis.

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Section: Discussionmentioning

confidence: 99%

“…Moreover, NCK1-AS1 has been proved to be related with the development of different cancers, including prostate cancer [ 11 ], osteosarcoma [ 12 ], cervical cancer [ 13 ], glioma [ 14 ], etc. Intriguingly, NCK1-AS1 contributes to the development of cancers by sponging miRNAs as a competing endogenous RNA (ceRNA).…”

Section: Introductionmentioning

confidence: 99%

NCK1-AS1 promotes the progression of melanoma by accelerating cell proliferation and migration via targeting miR-526b-5p/ADAM15 axis

et al. 2021

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“…Prostate cancer, a serious tumor type in men, makes no exception to the importance of lncRNA-mediated functions that relate to different hallmarks of cancer ( 11 ). Although TGF-β signaling does not seem to regulate expression of NCK1-AS1 , this lncRNA was highly expressed in prostate carcinomas and underexpressed in normal or even benign hyperplastic prostate tissue and seems to activate TGFB1 mRNA and TGF-β signaling via as yet unknown molecular mechanism ( 87 ). In contrast, the MIR100HG gene that was described in the lung cancer section was transcriptionally induced by TGF-β and formed a feed-forward signaling loop by facilitating TGFB1 mRNA stabilization and growth factor secretion by prostate cancer cells ( 46 ).…”

Section: Prostate Cancermentioning

confidence: 99%

Unboxing the network among long non-coding RNAs and TGF-β signaling in cancer

Rodrigues-Junior,

Moustakas

2024

ujms

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Deeper analysis of molecular mechanisms arising in tumor cells is an unmet need to provide new diagnostic and therapeutic strategies to prevent and treat tumors. The transforming growth factor β (TGF-β) signaling has been steadily featured in tumor biology and linked to poor prognosis of cancer patients. One pro-tumorigenic mechanism induced by TGF-β is the epithelial-to-mesenchymal transition (EMT), which can initiate cancer dissemination, enrich the tumor stem cell population, and increase chemoresistance. TGF-β signals via SMAD proteins, ubiquitin ligases, and protein kinases and modulates the expression of protein-coding and non-coding RNA genes, including those encoding larger than 500 nt transcripts, defined as long non-coding RNAs (lncRNAs). Several reports have shown lncRNAs regulating malignant phenotypes by directly affecting epigenetic processes, transcription, and post-transcriptional regulation. Thus, this review aims to update and summarize the impact of TGF-β signaling on the expression of lncRNAs and the function of such lncRNAs as regulators of TGF-β signaling, and how these networks might impact specific hallmarks of cancer.

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“…12 More studies indicated that NCK1-AS1 was involved in many signaling pathways, such as CDK and TGF-β1 signaling. 12,14 By analysis of TCGA dataset, we observed the significantly upregulated NCK1-AS1 in urothelial bladder carcinoma (TCGA-BLCA, see results: http://gepia.cancer-pku.cn/detail.php?gene=NCK1-AS1). MicroRNAs (miRNAs,~20 nt) are a class of non-coding small RNAs that are highly conserved in evolution.…”

Section: Introductionmentioning

confidence: 97%

<p>LncRNA NCK1-AS1 Promotes Cancer Cell Proliferation and Increase Cell Stemness in Urinary Bladder Cancer Patients by Downregulating miR-143</p>

Zhou¹,

Dai²,

Zhang³

et al. 2020

CMAR

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Background: Long noncoding RNAs (lncRNAs) play critical and complex roles in regulating various biological processes of cancers. Our study aimed to investigate the involvement of lncRNA NCK1-AS1 in urinary bladder cancer (UBC). Methods: qRT-PCR was used to detect the expression of lncRNA NCK1-AS1 and miR-143 in UBC tissues and cells. The dual-luciferase reporter system assays were used to confirm the interaction between NCK1-AS1 and miR-143, and flow cytometry assays were applied to examine the behavioral changes in HT-1376 and HT-1197 cell lines. Results: It was observed that NCK1-AS1 was up-regulated, while miR-143 was downregulated in tumor tissues than in adjacent healthy tissues of urinary bladder cancer (UBC) patients. A 5-year survival analysis showed that the survival rate of patients with high NCK1-AS1 level or low miR-143 level in tumor tissues appears relatively low. Correlation analysis revealed a significant inverse correlation between NCK1-AS1 and miR-143 in tumor tissues. Over-expression NCK1-AS1 reduced the expression level of miR-143, while elevating the level of miR-143 failed to affect NCK1-AS1 expression. NCK1-AS1 over-expression led to promoted proliferation and increased percentage of CD133+ (stemness) cells. Conclusion: Therefore, NCK1-AS1 promotes cancer cell proliferation and increases cell stemness in UBC patients by down-regulating miR-143.

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Altered expression of lncRNA NCK1‑AS1 distinguished patients with prostate cancer from those with benign prostatic hyperplasia

Cited by 7 publications

References 26 publications

NCK1-AS1 promotes the progression of melanoma by accelerating cell proliferation and migration via targeting miR-526b-5p/ADAM15 axis

NCK1-AS1 promotes the progression of melanoma by accelerating cell proliferation and migration via targeting miR-526b-5p/ADAM15 axis

Unboxing the network among long non-coding RNAs and TGF-β signaling in cancer

<p>LncRNA NCK1-AS1 Promotes Cancer Cell Proliferation and Increase Cell Stemness in Urinary Bladder Cancer Patients by Downregulating miR-143</p>

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