LINC01133 promotes the progression of cervical cancer by sponging miR-4784 to up-regulate AHDC1

Feng, Yan; Qu, Luyun; Wang, Xiuli; Liu, Chunyan

doi:10.1080/15384047.2019.1647058

Cited by 23 publications

(20 citation statements)

References 38 publications

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“…There is accumulating evidence that the downstream targets and signaling pathways regulated by LINC01133 contributes to the malignant behavior of multiple types of cancer cells. [29][30][31][32] In nonsmall cell lung carcinoma, LINC01133 suppresses the transcription of KLF2, P21, and E-cadherin by binding to EZH2 and LSD1, resulting in increased cancer cell growth and invasion. 33 In colon cancer, LINC01133 inhibits EMT and metastasis by interacting with SRSF6.…”

Section: Discussionmentioning

confidence: 99%

LINC01133 promotes hepatocellular carcinoma progression by sponging miR‐199a‐5p and activating annexin A2

Yin

Luo

et al. 2021

Clinical & Translational Med

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Background Long noncoding RNAs (lncRNAs) are functionally associated with cancer development and progression. Although gene copy number variation (CNV) is common in hepatocellular carcinoma (HCC), it is not known how CNV in lncRNAs affects HCC progression and recurrence. We aimed to identify a CNV‐related lncRNA involved in HCC progression and recurrence and illustrate its underlying mechanisms and prognostic value. Methods We analyzed the whole genome sequencing (WGS) data of matched cancerous and noncancerous liver samples from 49 patients with HCC to identify lncRNAs with CNV. The results were validated in another cohort of 238 paired HCC and nontumor samples by TaqMan copy number assay. We preformed Kaplan‐Meier analysis and log‐rank test to identify lncRNA CNV with prognostic value. We conducted loss‐ and gain‐of‐function studies to explore the biological functions of LINC01133 in vitro and in vivo. The competing endogenous RNAs (ceRNAs) mechanism was clarified by microRNA sequencing (miR‐seq), quantitative real‐time PCR (qRT‐PCR), western blot, and dual‐luciferase reporter assays. We confirmed the binding mechanism between lncRNA and protein by RNA pull‐down, RNA immunoprecipitation, qRT‐PCR, and western blot analyses. Results Genomic copy numbers of LINC01133 were increased in HCC, which were positively related with the elevated expression of LINC01133. Increased copy number of LINC01133 predicted the poor prognosis in HCC patients. LINC01133 overexpression in HCC cells promoted proliferation and aggressive phenotypes in vitro, and facilitated tumor growth and lung metastasis in vivo, whereas LINC01133 knockdown had the opposite effects. LINC01133 sponged miR‐199a‐5p, resulting in enhanced expression of SNAI1, which induced epithelial‐to‐mesenchymal transition (EMT) in HCC cells. In addition, LINC01133 interacted with Annexin A2 (ANXA2) to activate the ANXA2/STAT3 signaling pathway. Conclusions LINC01133 promotes HCC progression by sponging miR‐199a‐5p and interacting with ANXA2. LINC01133 CNV gain is predictive of poor prognosis in patients with HCC.

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Section: Discussionmentioning

confidence: 99%

LINC01133 promotes hepatocellular carcinoma progression by sponging miR‐199a‐5p and activating annexin A2

Yin

Luo

et al. 2021

Clinical & Translational Med

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“…in non-small-cell lung cancer [26,27], colorectal cancer [28] and osteosarcoma [29]. It could promote NSCLS cells' proliferation, migration and invasion through binding to EZH2 and LSD1 to repress KLF2, P21 and E-cadherin transcription [27].…”

Section: Discussionmentioning

confidence: 99%

“…There is accumulating evidence that the downstream targets and signaling pathways regulated by LINC01133 are involved in the malignant behavior of multiple types of cancer cells [26][27][28][29]. In non-small cell lung carcinoma, LINC01133 suppresses the transcription of KLF2, P21 and E-cadherin by binding to EZH2 and LSD1, resulting in increased cell growth and invasion [30].…”

Section: Discussionmentioning

confidence: 99%

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The Long Non-coding RNA LINC01133 Promotes Hepatocellular Carcinoma Progression by Sponging miR-199a-5p and Activating Annexin A2

Yin

Luo

et al. 2020

Preprint

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Background: Long non-coding RNAs (lncRNAs) have been found to be functionally associated with cancer development and progression. Although copy number variations (CNVs) are common in hepatocellular carcinoma (HCC), little is known about how CNVs in lncRNAs affect HCC progression and recurrence.Methods: We analyzed the whole genome sequencing (WGS) data of matched cancerous and non-cancerous liver samples from 49 patients with HCC to identify lncRNAs with CNVs. The results were validated in another cohort of 238 paired HCC and non-tumor samples by TaqMan copy number assay. Kaplan-Meier analysis and the log-rank test were performed to determine the prognostic value of CNVs in lincRNAs. Loss- and gain-of-function studies were conducted to determine the biological functions of LINC01133 in vitro and in vivo. The competing endogenous RNAs (ceRNAs) mechanism was clarified by microRNA sequencing (miR-seq), quantitative real-time PCR (qRT-PCR), western blot, and dual-luciferase reporter analyses. The protein binding mechanism was confirmed by RNA pull-down, RNA immunoprecipitation (RIP), qRT-PCR, and western blot analyses.Results: Genomic copy number of LINC01133 was increased in HCC, which is positively related with the elevated expression of LINC01133. Increased copy number of LINC01133 predicted the poor prognosis in HCC patients. LINC01133 overexpression promoted proliferation, colony formation, migration, and invasion in vitro, and facilitated tumor growth and lung metastasis in vivo, whereas LINC01133 knockdown had the opposite effects. Mechanistically, LINC01133 acted as a sponge of miR-199a-5p, resulting in enhanced expression of SNAI1, which induced epithelial-mesenchymal transition (EMT) in HCC cells. In addition, LINC01133 interacted with Annexin A2 (ANXA2) to activate ANXA2/STAT3 signaling pathway.Conclusions: LINC01133 promotes HCC progression by sponging miR-199a-5p and interacting with ANXA2. LINC01133 CNV gain is predictive of poor prognosis in HCC patients undergoing curative resection.

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“…LINC01133, a novel lncRNA, was first reported in 2015 to be highly expressed in lung squamous cell carcinoma (LSCC), but not in lung adenocarcinoma [ 27 ]. Recently, it has been verified that LINC01133 is involved in multiple types of malignant tumors, such as LSCC, osteosarcoma [ 20 ], cervical cancer [ 28 ], hepatocellular carcinoma [ 29 ], colorectal cancer (CRC) [ 30 ], and gastric carcinoma [ 31 ]. These studies collectively suggested that LINC01133 is an important regulator of cell proliferation and tumorigenesis, and may be a potential therapeutic target.…”

Section: Introductionmentioning

confidence: 99%

Tumor-derived exosomal long noncoding RNA LINC01133, regulated by Periostin, contributes to pancreatic ductal adenocarcinoma epithelial-mesenchymal transition through the Wnt/β-catenin pathway by silencing AXIN2

et al. 2021

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Pancreatic ductal adenocarcinoma (PDAC) is one of the most fatal malignancies and rapidly progressive diseases. Exosomes and long noncoding RNAs (lncRNAs) are emerging as vital mediators in tumor cells and their microenvironment. However, the detailed roles and mechanisms of exosomal lncRNAs in PDAC progression remain unknown. Here, we aimed to clarify the clinical significance and mechanisms of exosomal lncRNA 01133 (LINC01133) in PDAC. We analyzed the expression of LINC01133 in PDAC and found that exosomal LINC01133 expression was high and positively correlated with higher TNM stage and poor overall survival rate of PDAC patients. Further research demonstrated that Periostin could increase exosome secretion and then enhance LINC01133 expression. In addition, Periostin increased p-EGFR, p-Erk, and c-myc expression, and c-myc could bind to the LINC01133 promoter region. These findings suggested that LINC01133 can be regulated by Periostin via EGFR pathway activity. We also observed that LINC01133 promoted the proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT) of pancreatic cancer cells. We subsequently evaluated the effect of LINC01133 on the Wnt/β-catenin pathway and confirmed that LINC01133 can interact with Enhancer Of Zeste Homolog 2 (EZH2) and then promote H3K27 trimethylation. This can further silence AXIN2 and suppress GSK3 activity, ultimately activating β-catenin. Collectively, these data indicate that exosomal LINC01133 plays an important role in pancreatic tumor progression, and targeting LINC01133 may provide a potential treatment strategy for PDAC.

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LINC01133 promotes the progression of cervical cancer by sponging miR-4784 to up-regulate AHDC1

Cited by 23 publications

References 38 publications

LINC01133 promotes hepatocellular carcinoma progression by sponging miR‐199a‐5p and activating annexin A2

LINC01133 promotes hepatocellular carcinoma progression by sponging miR‐199a‐5p and activating annexin A2

The Long Non-coding RNA LINC01133 Promotes Hepatocellular Carcinoma Progression by Sponging miR-199a-5p and Activating Annexin A2

Tumor-derived exosomal long noncoding RNA LINC01133, regulated by Periostin, contributes to pancreatic ductal adenocarcinoma epithelial-mesenchymal transition through the Wnt/β-catenin pathway by silencing AXIN2

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