LINC00052 functions as a tumor suppressor through negatively modulating miR‐330‐3p in pancreatic cancer

Xiong, Xingcheng; Shi, Qiao; Yang, Xi; Wang, Weixing; Ji, Tao

doi:10.1002/jcp.28209

Cited by 26 publications

(17 citation statements)

References 28 publications

(34 reference statements)

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“…Furthermore, miRNAs have involved in lncRNAs. Xiong, X et al [27] demonstrated that linc00052 functioned as a tumor suppressor via negatively regulating miR-330-3p in pancreatic cancer. Instead, linc00858 exerted its function through the suppression of miR-22-3p to promote cells proliferation, migration and invasion [28].…”

Section: Discussionmentioning

confidence: 99%

Up-regulated Linc00472 suppresses development of lung cancer cell via inhibition of MiR-196b-5p

Mao¹,

Zhou²,

Li³

et al. 2019

Bioscience, Biotechnology, and Biochemistry

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The role of linc00472 in lung cancer (LC) has been rarely reported. We aimed to study the role of linc00472 in LC progression. Expressions of linc00472 and miR-196b-5p in LC cell lines were measured by qRT-PCR. The targeting relationship between linc00472 and miR-196b-5p was determined by Starbase and dual-luciferase reporter. The viability, migration, invasion, and apoptosis of LC cells were determined using CCK-8 assay, scratch test, transwell assay, and flow cytometry, respectively. The levels of epithelial-to-mesenchymal transition (EMT)-related proteins and apoptosis-related proteins in LC cells were determined by western blot. Downregulated linc00472 was observed in five LC cell lines. Linc00472 overexpression suppressed viability, migration, invasion and EMT process, but elevated apoptotic rate in LC cells. MiR-196b-5p mimic promoted viability, migration, invasion, and EMT process, but decreased apoptotic rate, which was reversed by up-regulated linc00472. Linc00472 functioned as a cancer suppressor via negatively regulating miR-196b-5p of LC cells.

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Section: Discussionmentioning

confidence: 99%

Up-regulated Linc00472 suppresses development of lung cancer cell via inhibition of MiR-196b-5p

Mao¹,

Zhou²,

Li³

et al. 2019

Bioscience, Biotechnology, and Biochemistry

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“…Then, online prediction and the dual luciferase reporter gene assay identified that HAGLR could directly bind to miR-330-3p, which was further found to be highly expressed in LC patients. miR-330-3p has been documented to serve as an oncogene in pancreatic cancer [27]. Importantly, previous studies have suggested that miR-330-3p could promote NSCLC LC progression by inhibiting malignant behaviors of LC cells including proliferation, invasion, migration and metastasis [28,29].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA HAGLR inhibits growth and metastasis and reduces stemness of lung cancer cells through the microRNA-330-3p/SLC34A2 axis

Yang¹,

Chen

Zhong

et al. 2020

Preprint

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Background Lung cancer (LC) remains a leading cause of cancer-related mortality worldwide. Long noncoding RNAs (lncRNAs) are crucial regulatory molecules in diverse pathological processes, including cancer progression. This study was conducted to probe the influence of lncRNA HAGLR on the growth, metastasis and stemness of LC cells. Methods Aberrantly expressed lncRNAs in LC tissues were screened out using microarray analysis. HAGLR expression in LC tissues and cells and in the paired normal ones was determined using RT-qPCR. Overexpression of HAGLR was administrated in H1299 and A549 cells to identify its function in the biological characteristics of LC cells. Sub-cellular localization of HAGLR was determined, and the downstream molecules involved in the HAGLR-mediated events were predicted on a bioinformation system and validated through dual luciferase reporter gene assay. Results HAGLR was poorly expressed in both LC tissues and cells. Overexpression of HAGLR inhibited viability, proliferation and metastasis, and reduced the stemness of H1299 and A549 cells. HAGLR up-regulated SLC34A2 expression through sponging miR-330-3p, leading to further inactivation of the Wnt/β-catenin signaling pathway. Artificial activation of the Wnt/β-catenin pathway recovered the viability and promoted metastasis of LC cells inhibited by HAGLR Conclusion HAGLR serves as a competing endogenous RNA for miR-330-3p to upregulate miR-330-3p expression and inactivate the Wnt/β-catenin pathway, leading to inhibited growth and metastasis and reduced stemness of LC cells.

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“…Upregulated LINC00472 suppressed the development of cell viability and promoted apoptosis of lung cancer cells by inhibiting miR‐196b‐5p, suggesting a possible therapeutic target in lung cancer treatment 74 . Xiong et al demonstrated that LINC00052 functioned as a tumor suppressor via negatively regulating miR‐330‐3p in pancreatic cancer 75 . It was proved that the LINC00472 expression level could be used as a better disease outcome maker in breast cancer 76 .…”

Section: Crndementioning

confidence: 99%

“…74 Xiong et al demonstrated that LINC00052 functioned as a tumor suppressor via negatively regulating miR-330-3p in pancreatic cancer. 75 It was proved that the LINC00472 expression level could be used as a better disease outcome maker in breast cancer. 76 Zou et al identified that LINC00472 upregulation prevents the cell invasion, metastasis, and growth in NCI-H1299 Cells.…”

Section: Linc00472mentioning

confidence: 99%

Long non‐coding RNAs as potential biomarkers in the prognosis and diagnosis of lung cancer: A review and target analysis

et al. 2020

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Long non-coding RNAs (lncRNA) have been emerged as a novel class of molecular regulators in cancer. They are dysregulated in many types of cancer; however, there is not enough knowledge available on their expression and functional profiles. Lung cancer is the leading cause of the cancer deaths worldwide. Generally, lncRNAs may be associated with lung tumor pathogenesis and they may act as biomarkers for the cancer prognosis and diagnosis. Compared to other invasive prognostic and diagnostic methods, detection of lncRNAs might be a user-friendly and noninvasive method. In this review article, we selected 27 tumor-associated lncRNAs by literature reviewing to further discussing in detail for using as diagnostic and prognostic biomarkers in lung cancer. Also, in an in silico target analysis, the "Experimentally supported functional regulation" approach of the LncTarD web tool was used to identifying the target genes and regulatory mechanisms of the selected lncRNAs. The reports on diagnostic and prognostic potential of all selected lncRNAs were discussed. However, the target genes and regulatory mechanisms of the 22 lncRNAs were identified by in silico analysis and we found the pathways that are controlled by each target group of lncRNAs. They use epigenetic mechanisms, ceRNA mechanisms, protein interaction and sponge mechanism. Also, 10, 23, 5, and 28 target genes for each of these mechanisms were identified, respectively. Finally, each group of target genes controls 50, 12, 7, and 2 molecular pathways, respectively. In conclusion, LncRNAs could be used as

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LINC00052 functions as a tumor suppressor through negatively modulating miR‐330‐3p in pancreatic cancer

Cited by 26 publications

References 28 publications

Up-regulated Linc00472 suppresses development of lung cancer cell via inhibition of MiR-196b-5p

Up-regulated Linc00472 suppresses development of lung cancer cell via inhibition of MiR-196b-5p

Long non-coding RNA HAGLR inhibits growth and metastasis and reduces stemness of lung cancer cells through the microRNA-330-3p/SLC34A2 axis

Long non‐coding RNAs as potential biomarkers in the prognosis and diagnosis of lung cancer: A review and target analysis

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