LINC01089 Inhibits Tumorigenesis and Epithelial–Mesenchymal Transition of Non-small Cell Lung Cancer via the miR-27a/SFRP1/Wnt/β-catenin Axis

Li, Xingkai; Lv, Fang; Li, Fang; Du, Minjun; Liang, Yicheng; Ju, Shaolong; Liu, Zixu; Zhou, Boxuan; Wang, Bing; Gao, Yushun

doi:10.3389/fonc.2020.532581

Cited by 15 publications

(10 citation statements)

References 29 publications

(30 reference statements)

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“…Previous studies have shown that LINC01089 was mainly located in the cytoplasm of NSCLC cells [ 21 ], suggesting that it may function as a molecular sponge. To delve into the mechanism of LINC01089 in regulating the biological behaviors of NSCLC cells, we used bioinformatics analysis tool StarBase V2.0 () to screen the potential downstream targets for LINC01089.…”

Section: Resultsmentioning

confidence: 99%

“…In breast cancer, LINC01089 functions as a tumor suppressor via regulating cell cycle regulators and wnt/β-catenin signaling [ 13 ]. A recent study also suggests that LINC01089 inhibits tumorigenesis and epithelial-mesenchymal transition of NSCLC via the miR-27a/SFRP1/Wnt/β-catenin axis [ 21 ]. These studies suggest that LINC01089 is a crucial regulator in Wnt/β-catenin signaling.…”

Section: Discussionmentioning

confidence: 99%

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RETRACTED ARTICLE: LINC01089 functions as a ceRNA for miR-152-3p to inhibit non‐small lung cancer progression through regulating PTEN

Zhang

et al. 2021

Cancer Cell Int

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Background Long non-coding RNAs (lncRNAs) have been reported to exert crucial functions in regulating the progression of human cancers. However, the function and mechanism of long intergenic non-protein coding RNA 01089 (LINC01089) in non-small cell lung cancer (NSCLC) have not been revealed. Methods The expression level of LINC01089, microRNA (miRNA, miR)-152-3p and phosphatase and tensin homolog deleted onc hromosome ten (PTEN) mRNA was detected by quantitative real-time PCR (qRT-PCR). After gain-of-function and loss-of-function models were established with NSCLC cell lines, the proliferation, migration and invasion of NSCLC cells were detected by cell counting kit-8 (CCK-8) assay, scratch healing assay, Transwell assay, respectively. Dual luciferase reporter assay was employed to validate the binding relationship between miR-152-3p and LINC01089 or the 3’UTR of PTEN. Western blot was used to detect PTEN expression in NSCLC cells after LINC01089 and miR-152-3p were selectively modulated. Results LINC01089 was down-regulated in NSCLC tissues and cells. Functional experiments showed that knockdown of LINC01089 could promote the proliferation, migration and invasion of NSCLC cells, while over-expression of LINC01089 had the opposite effects. miR-152-3p was identified as a functional target for LIN01089, and miR-152-3p could reverse the function of LINC01089. Additionally, LINC01089 could up-regulate the expression level of PTEN via repressing miR-152-3p. Conclusions Down-regulation of LINC01089 promoted the progression of NSCLC through regulating miR-152-3p/PTEN axis.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: LINC01089 functions as a ceRNA for miR-152-3p to inhibit non‐small lung cancer progression through regulating PTEN

Zhang

et al. 2021

Cancer Cell Int

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“…For example, MALAT1 ( 43 ), DGCR5 ( 44 ) and NCK1-AS1 ( 45 ) were found to be increased in NSCLC tissues and were associated with the oncogenicity of NSCLC. By contrast, LINC01089 ( 46 ), LINC01089 ( 47 ) and DHRS4-AS1 ( 48 ) are found to be decreased in NSCLC and could play anti-carcinogenic roles. However, the detailed roles of LINC01748 in NSCLC remain unclear; thus, there is an urgent requirement for further investigation.…”

Section: Discussionmentioning

confidence: 89%

Long non‑coding RNA LINC01748 exerts carcinogenic effects in non‑small cell lung cancer cell lines by regulating the microRNA‑520a‑5p/HMGA1 axis

Tan

et al. 2021

Int J Mol Med

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The important functions of long non-coding RNAs in the malignancy of non-small cell lung cancer (NSCLC) has been increasingly highlighted. However, whether LINC01748 functions in a crucial regulatory role still requires further research. The aim of the present study was to investigate the biological roles of LINC01748 in NSCLC. Furthermore, different experiments were utilized to investigate the mechanism of action of LINC01748 in 2 NSCLC cell lines. Reverse transcription-quantitative PCR was used to measure mRNA expression levels. Cell Counting Kit-8 assay, flow cytometry analysis and Transwell and Matrigel assays were also used to analyze, cell viability, apoptosis, and migration and invasion, respectively. A tumor xenograft model was used for in vivo experiments. RNA immunoprecipitation experiments, luciferase reporter assays and rescue experiments were used to investigate the mechanisms involved. Data from The Cancer Genome Atlas dataset and patients recruited into the present study showed that LINC01748 was overexpressed in NSCLC. Patients with high LINC01748 mRNA expression level had shorter overall survival rate compared with that in patients with low LINC01748 mRNA expression level. Then, knockdown of LINC01748 mRNA expression level reduced cell proliferation, migration and invasion, but increased cell apoptosis in vitro . Knockdown of LINC01748 also reduced tumor growth in vivo . Mechanistically, LINC01748 could act as a competing endogenous (ce)RNA to sponge microRNA(miR)-520a-5p, to increase the expression level of the target gene, high mobility group AT-hook 1 (HMGA1) in the NSCLC cell lines. Furthermore, rescue experiments illustrated that the functions exerted by LINC01748 knockdown were negated by miR-520a-5p inhibition or HMGA1 overexpression. In summary, LINC01748 acted as a ceRNA by sponging miR-520a-5p, leading to HMGA1 overexpression, thus increasing the aggressiveness of the NSCLC cells. Accordingly, targeting the LINC01748/miR-520a-5p/HMGA1 pathway may benefit NSCLC therapy.

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“…LINC01089 has been reported to negatively impact tumorigenesis and play a role in the inhibition of the Wnt/β-catenin signaling ( Table 3 ) [ 44 , 45 ]; this impact might be in part via the targeting of miRNAs, including miR-3187-3p [ 46 ] and miR-27a [ 47 ]. β-catenin is a driver gene in aggressive ACC subgroups [ 19 ].…”

Section: Resultsmentioning

confidence: 99%

Prediction of Adrenocortical Carcinoma Relapse and Prognosis with a Set of Novel Multigene Panels

Lin

et al. 2022

Cancers

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Effective assessment of adrenocortical carcinoma (ACC) prognosis is critical in patient management. We report four novel and robust prognostic multigene panels. Sig27var25, SigIQvar8, SigCmbnvar5, and SigCmbn_B predict ACC relapse at area under the curve (AUC) of 0.89, 0.79, 0.78, and 0.80, respectively, and fatality at AUC of 0.91, 0.88, 0.85, and 0.87, respectively. Among their 33 component genes, 31 are novel. They could be differentially expressed in ACCs from normal tissues, tumors with different severity (stages and lymph node metastasis), ACCs with TP53 mutations, and tumors with differentially expressed immune checkpoints (CTLA4, PD1, TGFBR1, and others). All panels correlate with reductions of ACC-associated CD8+ and/or NK cells. Furthermore, we provide the first evidence for the association of mesenchymal stem cells (MSCs) with ACC relapse (p = 2 × 10−6) and prognosis (p = 2 × 10−8). Sig27var25, SigIQvar8, SigCmbnvar5, and SigCmbn_B correlate with MSC (spearman r ≥ 0.53, p ≤ 1.38 × 10−5). Sig27var25 and SigIQvar8 were derived from a prostate cancer (PC) and clear cell renal cell carcinoma (ccRCC) multigene signature, respectively; SigCmbnvar5 and SigCmbn_B are combinations of both panels, revealing close relationships of ACC with PC and ccRCC. The origin of these four panels from PC and ccRCC favors their prognostic potential towards ACC.

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LINC01089 Inhibits Tumorigenesis and Epithelial–Mesenchymal Transition of Non-small Cell Lung Cancer via the miR-27a/SFRP1/Wnt/β-catenin Axis

Cited by 15 publications

References 29 publications

RETRACTED ARTICLE: LINC01089 functions as a ceRNA for miR-152-3p to inhibit non‐small lung cancer progression through regulating PTEN

RETRACTED ARTICLE: LINC01089 functions as a ceRNA for miR-152-3p to inhibit non‐small lung cancer progression through regulating PTEN

Long non‑coding RNA LINC01748 exerts carcinogenic effects in non‑small cell lung cancer cell lines by regulating the microRNA‑520a‑5p/HMGA1 axis

Prediction of Adrenocortical Carcinoma Relapse and Prognosis with a Set of Novel Multigene Panels

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