Long non‐coding <scp>RNA LINC01207</scp> promotes prostate cancer progression by downregulating <scp>microRNA</scp>‐1972 and upregulating <scp>LIM</scp> and <scp>SH3</scp> protein 1

Wang, Sugui; Qiu, Junyi; Wang, Liping; Wu, Zhi‐Ying; Zhang, Xianyun; Li, Qiang; Jiang, Fujin

doi:10.1002/iub.2327

Cited by 12 publications

(9 citation statements)

References 33 publications

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“…Several miRNA molecules and other proteins such as kallikreins have been proposed as PC biomarkers ( 6 ). In addition, LINC01207 was previously reported to be highly expressed in prostate cancer, as it could downregulate miR-1972 and upregulate LIM and SH3 protein 1 to promote PC progression ( 35 ). In the present study, LINC01207 seems to act as an oncogenic gene through modulating miR-1182/AKT3 axis.…”

Section: Discussionmentioning

confidence: 99%

LINC01207 promotes prostate cancer progression by sponging miR‑1182 to upregulate AKT3

et al. 2021

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Prostate cancer (PC) is recognized as a common malignancy in male patients. Long non-coding RNA (lncRNA) has been implicated in the development of PC. Recently, long intergenic non-protein coding RNA 1207 (LINC01207) has been reported to regulate the carcinogenesis of multiple cancer types. However, its role in the progression of PC remains to be determined. The aim of the present study was to investigate the expression profile, clinicopathological implication and molecular mechanism of action of LINC01207 in the progression of PC. LINC01207 expression levels were compared between PC tumor and paired normal tissue samples from The Cancer Genome Atlas. The expression of LINC01207 was further analyzed in PC cell lines and a normal prostatic cell line. The role of LINC01207 in proliferation, migration and invasion of PC cells was examined using small interfering RNA-mediated silencing. Western blot analysis was used to investigate the changes in protein levels underlying the mechanism of action of LINC01207. The role of LINC01207 in tumorigenesis was evaluated in a xenograft model. LINC01207 was upregulated in PC tumor samples from TCGA data compared with paired normal tissue. LINC01207 expression was significantly increased in PC cells and tumor tissues compared with in normal prostate cells (RWPE1) and normal prostate tissues, respectively. Furthermore, LINC01207 silencing inhibited PC cell proliferation and colony formation and induced apoptosis. Mechanistic experiments showed that LINC01207 promoted carcinogenesis by sponging miR-1182 to regulate the protein levels of AKT3 in PC cell lines. Thus, the findings of the present study indicated that LINC01207 might play a role in the tumorigenesis of PC and may serve as a therapeutic target for PC treatment.

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Section: Discussionmentioning

confidence: 99%

LINC01207 promotes prostate cancer progression by sponging miR‑1182 to upregulate AKT3

et al. 2021

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“…LncRNA LINC01207, located in the 4q32 genomic locus with three exons and two introns, has been reported to be upregulated in multiple types of cancer and associated with the prognosis of patients with poor survival (205)(206)(207)(208)(209). Recent studies have demonstrated that LINC01207 performs as an oncogenic lncRNA to promote cell growth, migration, invasion, and enhance apoptosis, as well as maintain stemness via ceRNA regulatory mechanism.…”

Section: Linc01207/mir-143-5p/agr2mentioning

confidence: 99%

Long Noncoding Competing Endogenous RNA Networks in Pancreatic Cancer

et al. 2021

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Pancreatic cancer (PC) is a highly malignant disease characterized by insidious onset, rapid progress, and poor therapeutic effects. The molecular mechanisms associated with PC initiation and progression are largely insufficient, hampering the exploitation of novel diagnostic biomarkers and development of efficient therapeutic strategies. Emerging evidence recently reveals that noncoding RNAs (ncRNAs), including long ncRNAs (lncRNAs) and microRNAs (miRNAs), extensively participate in PC pathogenesis. Specifically, lncRNAs can function as competing endogenous RNAs (ceRNAs), competitively sequestering miRNAs, therefore modulating the expression levels of their downstream target genes. Such complex lncRNA/miRNA/mRNA networks, namely, ceRNA networks, play crucial roles in the biological processes of PC by regulating cell growth and survival, epithelial–mesenchymal transition and metastasis, cancer stem cell maintenance, metabolism, autophagy, chemoresistance, and angiogenesis. In this review, the emerging knowledge on the lncRNA-associated ceRNA networks involved in PC initiation and progression will be summarized, and the potentials of the competitive crosstalk as diagnostic, prognostic, and therapeutic targets will be comprehensively discussed.

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“…The accumulated evidence demonstrates that cytoplasmic lncRNA acts as a ceRNA and decoy for certain miRNAs in human cancers. [30][31][32] Accordingly, a ceRNA model was utilized in the mechanistic studies. Using the miRDB, 36 miRNAs ( Figure 3D) were predicted as potential binding partners of LINC00519.…”

Section: Dovepressmentioning

confidence: 99%

<p>Long Intergenic Non-Protein Coding RNA 519 Promotes the Biological Activities of Tongue Squamous Cell Carcinoma by Sponging microRNA-876-3p and Consequently Upregulating MACC1</p>

Liu

Zhao

Wang

et al. 2020

OTT

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Long intergenic non-protein coding RNA 519 (LINC00519) promotes the development of lung squamous cell carcinoma. In this study, we detected the expression of LINC00519 in tongue squamous cell carcinoma (TSCC) and examined its clinical significance. Additionally, the regulatory effects of LINC00519 on behaviors of TSCC tumor cells were explored through functional experiments. Finally, mechanistic studies were performed to elucidate the molecular events underlying the tumor-promoting actions of LINC00519 in TSCC. Materials and Methods: The expression of LINC00519 in TSCC tissues and cell lines was determined using quantitative reverse transcription-polymerase chain reaction. Cell counting kit-8 assay, flow cytometric analysis, cell migration and invasion assays and xenograft tumor model analyses were used to detect TSCC cell proliferation, apoptosis, migration and invasion and in vivo tumor growth, respectively. Mechanistic studies were performed using bioinformatics analysis, RNA immunoprecipitation assay, luciferase reporter assay and rescue experiments. Results: LINC00519 was overexpressed in both TSCC tissues and cell lines. A high LINC00519 level was associated with poor overall survival in patients with TSCC. In vitro, LINC00519 played cancer-promoting roles in TSCC progression by facilitating cell proliferation, migration and invasion and restraining cell apoptosis. In vivo, LINC00519 downregulation resulted in decreased TSCC tumor growth. Mechanistically, LINC00519 acted as a competing endogenous RNA for microRNA-876-3p (miR-876-3p), which directly targets metastasis associated with colon cancer-1 (MACC1), in TSCC cells. LINC00519 upregulated the expression of MACC1 in TSCC cells by sequestering miR-876-3p. Rescue experiments further affirmed that miR-876-3p inhibition or MACC1 overexpression mitigated the inhibitory influences of LINC00519 depletion on cell proliferation, migration and invasion and neutralized the promoting actions of LINC00519 knockdown on cell apoptosis in TSCC. Conclusion: LINC00519 aggravated the oncogenicity of TSCC by regulating the miR-876-3p/MACC1 axis. Our findings suggest that the LINC00519/miR-876-3p/MACC1 pathway may be an underlying therapeutic target in TSCC.

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Long non‐coding RNA LINC01207 promotes prostate cancer progression by downregulating microRNA‐1972 and upregulating LIM and SH3 protein 1

Cited by 12 publications

References 33 publications

LINC01207 promotes prostate cancer progression by sponging miR‑1182 to upregulate AKT3

LINC01207 promotes prostate cancer progression by sponging miR‑1182 to upregulate AKT3

Long Noncoding Competing Endogenous RNA Networks in Pancreatic Cancer

<p>Long Intergenic Non-Protein Coding RNA 519 Promotes the Biological Activities of Tongue Squamous Cell Carcinoma by Sponging microRNA-876-3p and Consequently Upregulating MACC1</p>

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