lncRNA LINC00152 knockdown had effects to suppress biological activity of lung cancer via EGFR/PI3K/AKT pathway

Zhang, Yan; Cheng, Xiang; Wang, Yuling; Duan, Yuanyuan; Liu, Ci; Jin, Yan

doi:10.1016/j.biopha.2017.07.120

Cited by 53 publications

(48 citation statements)

References 36 publications

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“…This was revealed by the considerable decrease in EGFR, PI3K, and AKT activities and the epithelial intercellular transition via the suppression of fibronectin and vimentin downstream of the EGFR/PI3K/AKT signaling pathway to inhibit cell invasion and migration, in addition to an increase in P21 production to promote apoptosis. 41,42 This not only clarified the linc00152 mechanism related to the progression of NSCLC but also suggests that linc00152 is a potential therapeutic target. Several studies concluded that linc00152 expression is also upregulated in lung adenocarcinoma (LUAD) cells.…”

Section: Overexpression Of Linc00152 Enhances Cell Proliferation Imentioning

confidence: 83%

Improved characterization of the relationship between long intergenic non‐coding RNA Linc00152 and the occurrence and development of malignancies

Guo

Jiang

et al. 2019

Cancer Medicine

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Linc00152, located on chromosome 2p11.2, is a long intergenic non‐coding RNA molecule with 828 nucleotides that is highly expressed in many types of human tumor tissues, especially in malignant tumors of the digestive system. Linc00152 promotes the occurrence and development of tumors by increasing tumor cell proliferation, invasion, metastasis, and apoptosis. Additionally, linc00152 contributes to the carcinogenesis of several cancers, including gastric cancer, liver cancer, hepatocellular carcinoma, gallbladder cancer, clear cell renal cell carcinoma, and colorectal cancer, by disturbing various signaling pathways (eg PI3K/AKT, mTOR, IL‐1, and NOTCH 1 signaling pathways). High linc00152 expression levels are associated with chemoresistance as well as poor prognosis and shorter survival. Continual advances made in the relevant research have indicated that linc00152 may be useful as a new tumor molecular biomarker, applicable for tumor diagnosis, targeted therapy, and prognosis assessment. This review summarizes the progress in the research into the relationship between linc00152 and the occurrence and development of malignancies based on molecular functions, regulatory mechanisms, and clinical applications.

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Section: Overexpression Of Linc00152 Enhances Cell Proliferation Imentioning

confidence: 83%

Improved characterization of the relationship between long intergenic non‐coding RNA Linc00152 and the occurrence and development of malignancies

Guo

Jiang

et al. 2019

Cancer Medicine

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“…Long intergenic non-protein coding RNA 152 (LINC00152), also known as cytoskeleton regulator RNA, which is located on chromosome 2p11.2 (12), has been reported to be upregulated in colorectal cancer (13)(14)(15), breast cancer (16), lung cancer (17), tongue squamous cell carcinoma (18), gallbladder cancer (19) and renal cell carcinoma (20). These results emphasize the importance of the LINC00152 gene as an oncogene.…”

Section: Introductionmentioning

confidence: 99%

Long intergenic non‑protein coding RNA 152 promotes multiple myeloma progression by negatively regulating microRNA‑497

Zhang

et al. 2018

Oncol Rep

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Long intergenic non-protein coding RNA 152 (LINC00152, also known as cytoskeleton regulator RNA) is reportedly involved in the development and progression of various types of human malignancy. However, the functional role of LINC00152 in multiple myeloma (MM) and the underlying molecular mechanisms have remained elusive. The present study aimed to investigate the role of LINC00152 in the genesis of MM and the potential molecular mechanisms. It was identified that the expression of LINC00152 was significantly upregulated in plasma cells from patients with MM vs. healthy subjects, and that a high expression of LINC00152 was correlated with a shorter overall survival in patients with MM. Functional assays demonstrated that knockdown of LINC00152 by transfecting MM cells with LINC00152-specific short hairpin RNA expression plasmids significantly inhibited cell proliferation by inducing cell cycle arrest at the G 0 /G 1 phase. Furthermore, knockdown of LINC00152 promoted caspase-3/9 activity and apoptosis in MM cells. In addition, knockdown of LINC00152 significantly attenuated tumor growth in mice bearing a myeloma xenograft. A luciferase reporter assay indicated that microRNA (miR)-497 is a direct target of LINC00152, and its expression levels were inversely correlated with those of LINC00152 in MM tissues. Furthermore, repression of miR-497 partly abrogated the inhibitory effects of LINC00152 knockdown on MM cells. Collectively, the results indicated that LINC00152 has an oncogenic effect in MM by targeting miR-497, and may be a novel diagnostic marker and therapeutic target for MM.

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“…26 In the present study, we found that knockdown of LINC00152 inhibited the proliferation and induced the apoptosis in GC cells, which were consistent with previous studies in colon cancer, 27 gallbladder cancer 28 and lung cancer. 29 Furthermore, Chen et al 30 have reported that LINC00152 is correlated with tumor invasion depth, lymph node metastasis and TNM stage. In our study, we found that LINC00152 promoted GC cell proliferation and was associated with clinical stage and lymphatic metastasis, suggesting that LINC00152 may be an oncogenic lncRNA.…”

Section: Discussionmentioning

confidence: 99%

<p>Down-regulation of lncRNA LINC00152 Suppresses Gastric Cancer Cell Migration and Invasion Through Inhibition of the ERK/MAPK Signaling Pathway</p>

Shi

Sun²

2020

OTT

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The aim of this study was to explore the regulatory role and mechanism of long noncoding RNA LINC00152 in gastric cancer (GC) cells. Methods: LINC00152 expression in GC tissues and cells was detected by reverse transcription-polymerase chain reaction (qRT-PCR). MKN45 and MGC-803 cells were selected and assigned into different groups after transfection with si-LINC00152, activated ERK/MAPK signaling pathway (SA), or negative control. Cell proliferation, apoptosis, cycle, migration and invasion were assessed by CCK-8, flow cytometry, Transwell assay and Scratch test, respectively. Western blot analysis was conducted to detect the expression of E-cadherin, N-cadherin and ERK/MAPK signaling pathway protein. Results: Compared with the normal tissues, higher expression of LINC00152 was found in GC tissues and LINC00152 was remarkably correlative with clinical stage and lymphatic metastasis. LINC00152 expression in GC cells was higher than that in GES-1 cells. Compared with the NC group, the cell proliferation rate, cells in G2/M phase, migration and invasion abilities as well as the expression of N-cadherin and pERK -1/2 were significantly decreased, and the expression of E-cadherin, cells in G0/G1 phase and cell apoptosis rate were significantly increased in the si-LINC00152-1 group. ERK/MAPK signaling pathway activator SA could reverse the biological role of LINC00152 in GC cells. Conclusion: These results demonstrated that the interference of LINC00152 expression may inhibit the invasion and migration of GC cells by inhibiting the ERK/MAPK signaling pathway.

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lncRNA LINC00152 knockdown had effects to suppress biological activity of lung cancer via EGFR/PI3K/AKT pathway

Cited by 53 publications

References 36 publications

Improved characterization of the relationship between long intergenic non‐coding RNA Linc00152 and the occurrence and development of malignancies

Improved characterization of the relationship between long intergenic non‐coding RNA Linc00152 and the occurrence and development of malignancies

Long intergenic non‑protein coding RNA 152 promotes multiple myeloma progression by negatively regulating microRNA‑497

<p>Down-regulation of lncRNA LINC00152 Suppresses Gastric Cancer Cell Migration and Invasion Through Inhibition of the ERK/MAPK Signaling Pathway</p>

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