Neuregulin1 acts as a suppressor in human lung adenocarcinoma via AKT and ERK1/2 pathway

Wang, Youya; Ning, Zhifeng; Zhou, Xuefeng; Yang, Zhaohui; Tang, Huiping; Xu, Meifeng; Wang, Xianguo; Zhao, Jinping; Bai, Y.

doi:10.21037/jtd.2018.05.175

Cited by 11 publications

(8 citation statements)

References 37 publications

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“…We further assessed the role of SKA3 in EMT processes [22][23][24][25] but no associations were observed. Upon further analysis, we found that AKT activation strongly correlated with SKA3 expression, and that the expression of MMP following SKA3 silencing decreased in a manner that could be rescued by exogenous AKT overexpression, suggestive that SKA3 influences MMP-2, -7 and -9 to promote of LUAD occurrence and development [26][27][28][29][30][31][32]. These data further suggested that the selective modulation of SKA3 during EGFR-PI3K-AKT signaling in LUADs leads to EGF modulation, with no effects on HGF-signaling.…”

Section: Discussionmentioning

confidence: 94%

SKA3 promotes lung adenocarcinoma metastasis through the EGFR–PI3K–Akt axis

Chen

Lou

et al. 2020

Bioscience Reports

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The processes that lead to lung adenocarcinoma (LUAD) metastasis are poorly characterized. Spindle and kinetochore associated complex subunit 3 (SKA3) plays a key role in cervical cancer development, but its contribution to LUAD is unknown. Here, we found that SKA3 is overexpressed in LUAD and its expression correlates with lymph node metastasis and poor prognosis. SKA3 silencing experiments identified SKA3 as an oncogene that promotes the metastasis of LUAD cell lines and tissues. SKA3 was found to induce the expression of matrix metalloproteinase (MMP)-2, -7, and -9, which activate PI3K-AKT. SKA3 was also found to bind and activate EGFR to activate PI3K-AKT. In summary, we identify a role for SKA3 in LUAD metastasis through its ability to bind EFGR and activate PI3K-AKT signaling.

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Section: Discussionmentioning

confidence: 94%

SKA3 promotes lung adenocarcinoma metastasis through the EGFR–PI3K–Akt axis

Chen

Lou

et al. 2020

Bioscience Reports

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“…For example, LPCAT1 regulates LUAD metastasis by activating PI3K/AKT/MYC pathway 27 . NRG1 suppresses human lung adenocarcinoma through AKT and ERK1/2 pathway 28 . FLOT1 affects the progression of lung adenocarcinoma by regulating the Erk/Akt signaling pathway 29 .…”

Section: Discussionmentioning

confidence: 99%

Upregulation of LINC01426 promotes the progression and stemness in lung adenocarcinoma by enhancing the level of SHH protein to activate the hedgehog pathway

Liu

Yin

et al. 2021

Cell Death Dis

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Long noncoding RNAs (lncRNAs) play crucial roles in regulating a variety of biological processes in lung adenocarcinoma (LUAD). In our study, we mainly explored the functional roles of a novel lncRNA long intergenic non-protein coding RNA 1426 (LINC01426) in LUAD. We applied bioinformatics analysis to find the expression of LINC01426 was upregulated in LUAD tissue. Functionally, silencing of LINC01426 obviously suppressed the proliferation, migration, epithelial–mesenchymal transition (EMT), and stemness of LUAD cells. Then, we observed that LINC01426 functioned through the hedgehog pathway in LUAD. The effect of LINC01426 knockdown could be fully reversed by adding hedgehog pathway activator SAG. In addition, we proved that LINC01426 could not affect SHH transcription and its mRNA level. Pull-down sliver staining and RIP assay revealed that LINC01426 could interact with USP22. Ubiquitination assays manifested that LINC01426 and USP22 modulated SHH ubiquitination levels. Rescue assays verified that SHH overexpression rescued the cell growth, migration, and stemness suppressed by LINC01426 silencing. In conclusion, LINC01426 promotes LUAD progression by recruiting USP22 to stabilize SHH protein and thus activate the hedgehog pathway.

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“…For instance, neuregulin 1 (NRG1) might be an inhibitor in the progression of LUAD, and its function is related to the AKT and extracellular signal‐regulated protein kinase (ERK)1/2 pathways. 31 Flotillin‐1 (FLOT1) facilitates LUAD cell proliferation, invasion, and migration and inhibits cell apoptosis. In addition, FLOT1 induces epithelial–mesenchymal transition (EMT) and regulates the LUAD cell cycle via activating ERK/AKT cascades.…”

Section: Discussionmentioning

confidence: 99%

Silencing LINC01116 suppresses the development of lung adenocarcinoma via the AKT signaling pathway

Shang

et al. 2021

Thoracic Cancer

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Background: A growing body of evidence has proven that long noncoding ribonucleic acids (lncRNAs) are important epigenetic regulators that play crucial parts in the pathogenesis of human cancers. Previous studies have shown that long intergenic nonprotein coding RNA 01116 (LINC01116) is a carcinogen in several carcinomas; however, its function in lung adenocarcinoma (LUAD) has not been clarified. Here, we aimed to investigate the role of LINC01116 in LUAD. Methods: The relative expression levels of LINC01116 in LUAD cell lines and tissues were detected by quantitative reverse transcription polymerase chain reaction. A Kaplan-Meier survival analysis was performed using patient information from the Gene Expression Profiling Interactive Analysis (GEPIA) database. LUAD proliferation, invasion, migration, and apoptosis were measured by performing cell counting kit-8, colony formation, transwell, wound healing, and flow cytometric assays. A xenograft animal experiment was performed to investigate the effect of LINC01116 in vivo. Protein kinase B (AKT) signaling pathway-related protein expressions were tested by Western blot assay. Results: LINC01116 expression was upregulated in LUAD cells and tissues. The lossof-function experiments on LUAD cells revealed that silencing LINC01116 expression could decrease cell viability both in vitro and in vivo. Furthermore, silencing LINC01116 inhibited LUAD cell invasion and migration and induced cell apoptosis. Mechanically, silencing LINC01116 significantly decreased p-AKT protein levels, and an AKT pathway stimulator could rescue the suppressive effects of small interfering LINC011116-specific RNAs on LUAD development. Conclusions: Our study demonstrated that silencing LINC01116 suppresses the development of LUAD via the AKT signaling pathway.

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Neuregulin1 acts as a suppressor in human lung adenocarcinoma via AKT and ERK1/2 pathway

Abstract: The current results suggested that NRG1 might be a suppressor in the development of LUAD, and its function was related to AKT and ERK1/2 pathway.

Cited by 11 publications

References 37 publications

SKA3 promotes lung adenocarcinoma metastasis through the EGFR–PI3K–Akt axis

SKA3 promotes lung adenocarcinoma metastasis through the EGFR–PI3K–Akt axis

Upregulation of LINC01426 promotes the progression and stemness in lung adenocarcinoma by enhancing the level of SHH protein to activate the hedgehog pathway

Silencing LINC01116 suppresses the development of lung adenocarcinoma via the AKT signaling pathway

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