miR-340 Restrains the Growth of Lung Cancer Cells Through Mitogen-Activated Protein Kinase (MAPK) Signaling

2021 ◽  
Vol 11 (5) ◽  
pp. 963-969
Author(s):  
Wenhong Zheng ◽  
Wenrui Xie ◽  
Lijuan Fu ◽  
Zhengqi Fu
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cellular Proliferation ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Lung Cancer Cells ◽  
Luciferase Assay ◽  
Knock Out ◽  
Novel Target

The lung cancer was most deadly tumor in the world and the suvival rate needs to be improved clinically and urgently. The abnormal miR-340 expression is found in several solid tumors. Our study was aimed to explore miR-340’s role in lung cancer. 14 cases of patients with lung cancer was selected to measure miR-340 level by RT-PCR and analyze its correlation with clinical characteristics. The relation between the miR-340 and DICER1 was detected by dual luciferase assay and cell proliferation was measured by MTT assay along with analysis of cell migration and invasive by Scratch-Wound experiment. The miR-340 in lung cancer cells was reduced significantly and DICER1 was predicted to be a potential target of miR-340. DICER1 level was found to be negatively related with miR-340 level. The DICER1 as the direct target gene of miR-340 was conducive to improve miR-340 function through overexpression and knock-out experiment further. Abnormal miR-340 level affected lung cancer cell proliferation and migration as well as MAPK signaling. miR-340 could affect the biological morphology and transformation of physiological function of lung cancer cells mainly through restraining the expression of apoptosis and prompting the cellular proliferation, indicating that it might be a novel target to improve the treatment of lung cancer.

scholarly journals miR-16 regulates proliferation and invasion of lung cancer cells via the ERK/MAPK signaling pathway by targeted inhibition of MAPK kinase 1 (MEK1)

2019 ◽  
Vol 47 (10) ◽  
pp. 5194-5204 ◽  
Author(s):  
TianMing Chen ◽  
Qi Xiao ◽  
XiaoJun Wang ◽  
ZhongQiu Wang ◽  
JingWen Hu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Mapk Signaling ◽  
Lung Cancer Cells ◽  
Lung Cancer Cell ◽  
Regulatory Relationship ◽  
Mapk Kinase ◽  
Erk Mapk ◽  
Proliferation And Invasion

Objective The ERK/MAPK signaling pathway regulates cell proliferation and invasion. MAPK kinase 1 (MEK1) is a protein kinase upstream of ERK that can activate the pathway. Expression of microRNA (miR)-16 in lung cancer tissues is decreased. The aim of this study was to determine roles of miR-16 in proliferation and invasion of lung cancer cells. Methods We used a luciferase reporter assay to determine a regulatory relationship between miR-16 and MEK1 and assessed expression of MEK1 in normal lung cells and lung cancer cell lines. Plate cloning, flow cytometry, and Transwell experiments demonstrated the proliferation and invasion ability of cells transfected with wild-type and mutant MEK1. Results We confirmed a regulatory relationship between miR-16 and MEK1 mRNA. Expression of miR-16 was decreased and that of MEK1 and p-ERK1/2 were increased in lung cancer cell lines compared with normal cells. Transfection with miR-101 mimic or small interfering (si)-MEK1 significantly downregulated expression of MEK1 and p-ERK1/2 in Anip973 cells. Conclusions Decreased miR-16 expression may play a role in upregulating expression of MEK1 and promoting proliferation and invasion of lung cancer cells. Overexpression of miR-16 downregulated the ERK/MAPK pathway by inhibiting MEK1 expression, attenuating clone formation and invasion, and inhibiting cell proliferation.

scholarly journals FBXW7-mediated ERK3 degradation regulates the proliferation of lung cancer cells

2022 ◽  
Author(s):  
Hyun-Jung An ◽  
Cheol-Jung Lee ◽  
Ga-Eun Lee ◽  
Youngwon Choi ◽  
Dohyun Jeung ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
E3 Ligase ◽  
Degradation Pathway ◽  
S Phase ◽  
Mitogen Activated Protein Kinase ◽  
Lung Cancer Cells ◽  
Migration And Invasion

AbstractExtracellular signal-regulated kinase 3 (ERK3) is an atypical member of the mitogen-activated protein kinase (MAPK) family, members of which play essential roles in diverse cellular processes during carcinogenesis, including cell proliferation, differentiation, migration, and invasion. Unlike other MAPKs, ERK3 is an unstable protein with a short half-life. Although deubiquitination of ERK3 has been suggested to regulate the activity, its ubiquitination has not been described in the literature. Here, we report that FBXW7 (F-box and WD repeat domain-containing 7) acts as a ubiquitination E3 ligase for ERK3. Mammalian two-hybrid assay and immunoprecipitation results demonstrated that ERK3 is a novel binding partner of FBXW7. Furthermore, complex formation between ERK3 and the S-phase kinase-associated protein 1 (SKP1)-cullin 1-F-box protein (SCF) E3 ligase resulted in the destabilization of ERK3 via a ubiquitination-mediated proteasomal degradation pathway, and FBXW7 depletion restored ERK3 protein levels by inhibiting this ubiquitination. The interaction between ERK3 and FBXW7 was driven by binding between the C34D of ERK3, especially at Thr417 and Thr421, and the WD40 domain of FBXW7. A double mutant of ERK3 (Thr417 and Thr421 to alanine) abrogated FBXW7-mediated ubiquitination. Importantly, ERK3 knockdown inhibited the proliferation of lung cancer cells by regulating the G1/S-phase transition of the cell cycle. These results show that FBXW7-mediated ERK3 destabilization suppresses lung cancer cell proliferation in vitro.

Knockdown CYP2S1 inhibits lung cancer cells proliferation and migration

2021 ◽  
pp. 1-9
Author(s):  
Huan Guo ◽  
Baozhen Zeng ◽  
Liqiong Wang ◽  
Chunlei Ge ◽  
Xianglin Zuo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Lung Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

BACKGROUND: The incidence of lung cancer in Yunnan area ranks firstly in the world and underlying molecular mechanisms of lung cancer in Yunnan region are still unclear. We screened a novel potential oncogene CYP2S1 used mRNA microassay and bioinformation database. The function of CYP2S1 in lung cancer has not been reported. OBJECTIVE: To investigate the functions of CYP2S1 in lung cancer. METHODS: Immunohistochemistry and Real-time PCR were used to verify the expression of CYP2S1. Colony formation and Transwell assays were used to determine cell proliferation, invasion and migration. Xenograft assays were used to detected cell growth in vivo. RESULTS: CYP2S1 is significantly up-regulated in lung cancer tissues and cells. Knockdown CYP2S1 in lung cancer cells resulted in decrease cell proliferation, invasion and migration in vitro. Animal experiments showed downregulation of CYP2S1 inhibited lung cancer cell growth in vivo. GSEA analysis suggested that CYP2S1 played functions by regulating E2F targets and G2M checkpoint pathway which involved in cell cycle. Kaplan-Meier analysis indicated that patients with high CYP2S1 had markedly shorter event overall survival (OS) time. CONCLUSIONS: Our data demonstrate that CYP2S1 exerts tumor suppressor function in lung cancer. The high expression of CYP2S1 is an unfavorable prognostic marker for patient survival.

scholarly journals MiR-107 inhibits proliferation of lung cancer cells through regulating TP53 regulated inhibitor of apoptosis 1 (TRIAP1)

2017 ◽  
Vol 12 (1) ◽  
pp. 200-205 ◽  
Author(s):  
Bing Wang ◽  
Zhanjie Zuo ◽  
Fang Lv ◽  
Liang Zhao ◽  
Minjun Du ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Western Blot ◽  
Cancer Cells ◽  
A549 Cells ◽  
Lung Cancer Cells ◽  
Pcr Analysis ◽  
Aberrant Expression ◽  
Small Interference Rna ◽  
Qrt Pcr

AbstractAimsAccumulating evidence indicates that aberrant expression of miR-107 plays a crucial role in cancers. This study aims to display the function of miR-107 and its novel target genes in the progression of lung cancer.Methods and MaterialMiR-107 or miR-107 inhibitor was transfected into lung cancer cells A549. The levels of miR-107 and TP53 regulated inhibition of apoptosis 1 (TRIAP1) were examined by quantitative real-time Polymerase Chain Reaction (qRT-PCR) analysis and Western Blot. Functionally, MTT and colony formation assays were carried out to test the effect of miR-107 inhibitor and/or small interference RNA (siRNA) targeting TRIAP1 mRNA on proliferation of lung cancer cells. Levels of miR-107 or TRIAP1 were detected in clinical lung cancer samples by using qRT-PCR analysis.ResultsQRT-PCR analysis revealed that miR-107 inhibitor or miR-107 was successfully transfected into A549 cells. Western Blot indicated that miR-107 decreased the expression of TRIAP1 protein in the cells. In contrast, miR-107 inhibitor augmented the levels of TRIAP1 protein. Functionally, miR-107 inhibitor remarkably suppressed A549 cell proliferation, whereas, TRIAP1 siRNAs could abrogate the miR-107 inhibitor-induced proliferation of cells. Then, we validated that TRIAP1 was increased in clinical lung cancer samples. MiR-107 expression was negatively related to TRIAP1 expression in clinical lung cancer samples.ConclusionsMiR-107 suppresses cell proliferation by targeting TRIAP1 in lung cancer. Our finding allows new insights into the mechanisms of lung cancer that is mediated by miR-107.

Effect of Curcumin Coated with Polymethyl Methacrylate Nanoparticles on Lung Cancer Cells

2020 ◽  
Vol 12 (8) ◽  
pp. 1015-1021
Author(s):  
Ximiao Ma ◽  
Fangyong Fu
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Polymethyl Methacrylate ◽  
Drug Loading ◽  
Lung Cancer Cells ◽  
Caspase 9 ◽  
Incidence And Mortality ◽  
High Incidence ◽  
Related Proteins

Lung cancer is a malignant tumor with an extremely high incidence and mortality rate in clinical practice and its pathogenesis remains unclear at present. Currently, the methods for treating this disease have relatively high limitations. However, with the gradual maturity and application of nanotechnology, a number of studies have pointed out that polymethyl methacrylate nanoparticles (PMMA-NPs) encapsulated with curcumin (Cur) possibly becomes a new and effective scheme for treating lung cancer. First of all, Cur-PMMA-NPs were prepared. Their sizes were determined by characterization techniques, and their effects on lung cancer cells A549 were detected by Cell proliferation experiment and flow cytometry. The expression of apoptosis-related proteins in the cells was detected by Western blotting. The results showed that polyacrylic acid (PAA)-Cur-PMMA-NPs had a particle size of (215.00±6.00) nm. The drug loading rate and the encapsulation rate of nanospheres were remarkably higher than those of free Cur (P < 0.05). After the intervention of PAA-Cur-PMMA-NPs in the cells, the cell proliferation and the Bcl-2 expression reduced, while the apoptotic rate and the expression of Bax, Caspase-3, and Caspase-9 increased (P < 0.05). Accordingly, Cur-PMMA-NPs can inhibit lung cancer cells from growth and induce their apoptosis, so they are expected to become an effective intervention measure to improve the therapeutic effect on lung cancer in the future.

scholarly journals Aptamer-miR-34c Conjugate Affects Cell Proliferation of Non-Small-Cell Lung Cancer Cells

2018 ◽  
Vol 13 ◽  
pp. 334-346 ◽  
Author(s):  
Valentina Russo ◽  
Alessia Paciocco ◽  
Alessandra Affinito ◽  
Giuseppina Roscigno ◽  
Danilo Fiore ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung

scholarly journals ZEB1 suppression sensitizes KRAS mutant cancers to MEK inhibition by an IL17RD-dependent mechanism

2019 ◽  
Vol 11 (483) ◽  
pp. eaaq1238 ◽  
Author(s):  
David H. Peng ◽  
Samrat T. Kundu ◽  
Jared J. Fradette ◽  
Lixia Diao ◽  
Pan Tong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Protein Kinase ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Mapk Signaling ◽  
Lung Tumors ◽  
Mitogen Activated Protein Kinase ◽  
Mek Inhibition ◽  
Mitogen Activated Protein

Mitogen-activated protein kinase (MAPK) kinase (MEK) inhibitors have failed to show clinical benefit in Kirsten rat sarcoma (KRAS) mutant lung cancer due to various resistance mechanisms. To identify differential therapeutic sensitivities between epithelial and mesenchymal lung tumors, we performed in vivo small hairpin RNA screens, proteomic profiling, and analysis of patient tumor datasets, which revealed an inverse correlation between mitogen-activated protein kinase (MAPK) signaling dependency and a zinc finger E-box binding homeobox 1 (ZEB1)–regulated epithelial-to-mesenchymal transition. Mechanistic studies determined that MAPK signaling dependency in epithelial lung cancer cells is due to the scaffold protein interleukin-17 receptor D (IL17RD), which is directly repressed by ZEB1. Lung tumors in multiple Kras mutant murine models with increased ZEB1 displayed low IL17RD expression, accompanied by MAPK-independent tumor growth and therapeutic resistance to MEK inhibition. Suppression of ZEB1 function with miR-200 expression or the histone deacetylase inhibitor mocetinostat sensitized resistant cancer cells to MEK inhibition and markedly reduced in vivo tumor growth, showing a promising combinatorial treatment strategy for KRAS mutant cancers. In human lung tumor samples, high ZEB1 and low IL17RD expression correlated with low MAPK signaling, presenting potential markers that predict patient response to MEK inhibitors.

scholarly journals Inhibition of HERG1 K+ channel protein expression decreases cell proliferation of human small cell lung cancer cells

2011 ◽  
Vol 463 (2) ◽  
pp. 365-376 ◽  
Author(s):  
Günter Glassmeier ◽  
Kathrin Hempel ◽  
Iris Wulfsen ◽  
Christiane K. Bauer ◽  
Udo Schumacher ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
K Channel ◽  
Small Cell Lung
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