RETRACTED ARTICLE: LINC00665/miR-9-5p/ATF1 is a novel axis involved in the progression of colorectal cancer

Zhao, Xuhong; Weng, Wenhao; Yin, Lu; Pan, Weijie; Li, Zhi; Sun, Fenyong

doi:10.1007/s13577-020-00393-z

Cited by 26 publications

(27 citation statements)

References 44 publications

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“…Previous studies have shown that the expression differences of lncRNAs were important mechanisms of the initiation and progression of cancer (16,17). In the present studies, it has been shown that LINC00665 performed the different biological functions in different types of tumors, and some scholars have reported it could act as an oncogene to promote the proliferation and migration of tumor (18)(19)(20). However, the biological functions and molecular mechanisms of LINC00665 in PCa cell lines need to be further investigated.…”

Section: Introductionmentioning

confidence: 69%

“…Based on the next-generation sequencing of PCa tissues to an indepth exploration of PCa tumor-related lncRNAs in the Chinese population, these studies focused on the molecular characteristics and functional mechanisms to better understand the biological behaviors of PCa cells, find new targets for the treatment of PCa, and provide evidence for the clinical diagnosis and new drug development of PCa (25,26). LINC00665 has been discovered for an extended period of time and is engaged in many physiological and pathological processes including the progression of tumors (18)(19)(20). In this study, to explore the function of LINC00665 in the malignant progression of PCa, we performed qRT-PCR assay and detected the up-regulated LINC00665 expression level in PCa tissues.…”

Section: Discussionmentioning

confidence: 99%

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Up-Regulation of LINC00665 Facilitates the Malignant Progression of Prostate Cancer by Epigenetically Silencing KLF2 Through EZH2 and LSD1

et al. 2021

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This study aimed to explore the function of LINC00665 on the proliferation and metastasis of prostate cancer (PCa), and the potential regulatory mechanisms were also investigated. The expression level of LINC00665 in 50 pairs of PCa tissues and adjacent ones was studied by qRT-PCR, and the associations between LINC00665 and clinicopathological characteristics of PCa patients were analyzed. Control group (sh-NC) and LINC00665 knock-down group (sh-LINC00665) were set in 22RV1 and DU145 cells, respectively. The biological functions of LINC00665 in PCa cell lines were assessed by CCK-8, EdU, Transwell assays, and the nude mouse xenograft model was used to evaluate the tumorigenicity in vivo. In addition, qRT-PCR, Western Blot, RIP and ChIP assays were also used to determine the regulation mechanism of LINC00665 in PCa cell lines. In this study, our results showed that LINC00665 expression level in PCa cancer tissues was significantly up-regulated, compared with that in adjacent ones. Besides, similar results were found in PCa cell lines. Knock-down of LINC00665 significantly attenuated the proliferation and migration ability in 22RV1 and DU145 cells, compared to sh-NC. Mechanically, LINC00665 could interact with EZH2 and LSD1, recruiting them to KLF2 promoter region to inhibit its transcription. Moreover, the tumor-suppressive effects mediated by sh-LINC00665 were significantly reversed through the down-regulation of KLF2. Also, the suppression of LINC00665 impaired tumor growth of PCa in vivo. In summary, LINC00665 exerted the oncogenic functions in PCa cell lines by epigenetically silencing KLF2 expression by binding to EZH2 and LSD1, illuminating a novel mechanism of LINC00665 in the malignant progression of PCa and furnishing a prospective therapeutic biomarker to combat PCa.

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Section: Introductionmentioning

confidence: 69%

Section: Discussionmentioning

confidence: 99%

Up-Regulation of LINC00665 Facilitates the Malignant Progression of Prostate Cancer by Epigenetically Silencing KLF2 Through EZH2 and LSD1

et al. 2021

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“…31 A recent study found that LINC00665 promoted the proliferation, migration and invasion of colorectal cancer cells, and also inhibited cell apoptosis by sponging miR-9-5p. 32 Similarly, another group indicated that LINC00665 is involved in NF-jB signaling activation in hepatocellular carcinoma cells. 33 LINC00665 also encodes a micropeptide, cellular inhibitor of protein phosphatase 2A binding peptide (CIP2A-BP), whose translation was shown to be downregulated by transforming growth factor-b (TGF-b) in breast cancer cell lines.…”

Section: Discussionmentioning

confidence: 99%

Autophagy-related long non-coding RNA signature for ovarian cancer

2020

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Objective Ovarian cancer (OC) affects nearly 22,000 women annually in the United States and ranks fifth in cancer deaths, largely because of being diagnosed at an advanced stage. Autophagy is the cellular process of self-degrading damaged or degenerate proteins and organelles. Long non-coding RNAs (lncRNAs) are a group of RNA molecules whose transcripts are greater than 200 nt but are not translated into proteins. However, just a small number of autophagy-related lncRNAs have been explored in depth. Methods We used RNA sequencing data from The Cancer Genome Atlas (TCGA) and autophagy datasets to identify dysfunctional autophagy-related lncRNAs and provide potential useful biomarkers for OC diagnosis and prognosis. Results Seventeen differentially expressed lncRNAs (AC010186.3, AC006001.2, LBX2-AS1, SNHG17, AC011445.1, AC083880.1, MIR193BHG, AC025259.3, HCG14, AC007114.1, AC108673.2, USP30-AS1, AC010336.5, LINC01132, AC006333.2, LINC00665 and AC027348.1) were selected as independent prognostic factors for OC patients. Functional annotation of the data was performed through gene set enrichment analysis (GSEA). The results suggested that the high-risk group was mainly enriched in specific tumor-related and metabolism pathways. Conclusion Based on the online databases, we identified novel autophagy-related lncRNAs for the prognosis of ovarian cancer.

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“…This study demonstrated that LINC00665 knockdown caused a reduction in the expression of cyclin D1, CDK4, and p-Rb. Caspase-3 and caspase-9 play an important role in the activation of downstream DNA cleavage molecules [ 31 ]. Activated caspases are an important way to induce apoptosis in cancer cells.…”

Section: Discussionmentioning

confidence: 99%

“…Accumulating evidence indicates that lncRNAs are used as ceRNAs of endogenous miRNAs to bind to miRNAs, and this function competitively inhibits the binding of miRNAs to their targets. A recent study showed that LINC00665 sponges miR-9-5p to further promote CRC progression by increasing ATF1 expression [ 31 ]. Similarly, we provide novel evidence of a ceRNA regulatory network in which LINC00665 functions as a miRNA sponge.…”

Section: Discussionmentioning

confidence: 99%

Long intergenic noncoding RNA 00665 promotes proliferation and inhibits apoptosis in colorectal cancer by regulating miR-126-5p

Shan

Han

et al. 2021

Aging

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Long intergenic noncoding RNAs (lincRNAs) regulate a series of biological processes, and their anomalous expression plays critical roles in the progression of multiple malignancies, including colorectal cancer (CRC). Although many studies have reported the oncogenic function of LINC00665 in multiple cancers, few studies have explored its role in CRC. The aim of this study was to assess the effect of LINC00665 on the malignant behaviors of CRC and explore the underlying regulatory mechanism of LINC00665. LINC00665 was significantly upregulated in CRC. A loss-of-function assay revealed that LINC00665 downregulation inhibited the proliferation and promoted the apoptosis of CRC cells, which was mediated by cyclin D1, CDK4, caspase-9 and caspase-3. Through mechanistic exploration, we found that miR-126-5p directly bound to LINC00665. Moreover, LINC00665 and miR-126-5p both regulated PAK2 and FZD3 expression. Mechanistically, miR-126-5p was predicted and further verified as a target of both PAK2 and FZD3. These findings demonstrate that LINC00665 might play an important pro-proliferative and antiapoptotic role in CRC and might be a potential biomarker and a new therapeutic target for CRC.

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RETRACTED ARTICLE: LINC00665/miR-9-5p/ATF1 is a novel axis involved in the progression of colorectal cancer

Cited by 26 publications

References 44 publications

Up-Regulation of LINC00665 Facilitates the Malignant Progression of Prostate Cancer by Epigenetically Silencing KLF2 Through EZH2 and LSD1

Up-Regulation of LINC00665 Facilitates the Malignant Progression of Prostate Cancer by Epigenetically Silencing KLF2 Through EZH2 and LSD1

Autophagy-related long non-coding RNA signature for ovarian cancer

Long intergenic noncoding RNA 00665 promotes proliferation and inhibits apoptosis in colorectal cancer by regulating miR-126-5p

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