scholarly journals Inhibition of ITCH Suppresses Proliferation and Induces Apoptosis of Lung Cancer Cells

2018 ◽  
Vol 48 (4) ◽  
pp. 1703-1709 ◽  
Author(s):  
Peng-Fei Li ◽  
Qi-Gang Zhang
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Cancer Proliferation ◽  
Flow Cytometric ◽  
Tumor Tissues ◽  
Proliferation And Apoptosis ◽  
Underlying Mechanisms ◽  
Cancer Tissues ◽  
Proliferation And Invasion

Background/Aims: The E3 ubiquitin ligase ITCH plays an important role in invasive and metastatic cancers. However, the role of ITCH in the progression of lung cancer has not been fully described. Methods: Real-time PCR was used to detect the expression of ITCH mRNA in the tumor tissues and paracarcinoma tissues from 32 patients with lung cancer. SiRNA was used to inhibit the expression of ITCH in two lung cancer cell lines, H1975 and Calu3 and the cell proliferation and apoptosis were measured by MTT and flow cytometric assay. In addition, to further investigate whether ITCH affected the apoptosis of cancer cells and its underlying mechanisms, the expression of important markers of apoptosis and invasion in lung cancer cells were detected by Western blot. Results: The study showed significant increments in the expression of ITCH in lung cancer tissues (p< 0.001). ITCH siRNA effectively inhibited the proliferation and invasion of the lung cancer cells and promoted cell apoptosis. Molecular analysis further showed significant reductions in the expression of Bcl2, MMP2, MMP9 and β-catenin and an increase in the expression of Bax and E-cadherin in the lung cancer cells with ITCH deficiency. Conclusions: Inhibition of ITCH might suppress lung cancer proliferation and invasion via regulation of MMPs, EMT and Bcl2/Bax signaling pathway.

scholarly journals FBXL19-AS1 exerts oncogenic function by sponging miR-431-5p to regulate RAF1 expression in lung cancer

2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Qian Jiang ◽  
Li Cheng ◽  
Daiyuan Ma ◽  
Yanli Zhao
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Molecular Mechanism ◽  
Lung Cancer Cells ◽  
Downstream Target ◽  
Non Coding Rna ◽  
Tumor Tissues ◽  
Inhibition Of Angiogenesis ◽  
Proliferation And Metastasis ◽  
Cancer Tissues

Abstract Lung cancer is the leading cause of cancer-related mortality worldwide, characterized by uncontrolled proliferation and metastasis of lung cancer cells. Tumor angiogenesis plays a key role in proliferation and metastasis in cancers, and is an essential component in microenvironment. It has been reported that long non-coding RNA FBXL19-AS1 plays an oncogenic role in colorectal cancer. However, the molecular mechanism of FBXL19-AS1 in lung cancer has not been fully elucidated. In the present study, we found that FBXL19-AS1 expression was up-regulated in lung cancer tissues and cell lines. FBXL19-AS1 knockdown inhibited cell proliferation, migration, invasion, and angiogenesis in lung cancer cells. Molecular mechanism exploration uncovered that FBXL19-AS1 acted as a molecular sponge of miR-431-5p and that RAF1 was a downstream target of miR-431-5p in lung cancer. Moreover, there was a negative association between miR-431-5p expression and FBXL19-AS1 or RAF1 expression in tumor tissues. Through rescue experiments, we discovered that overexpression of RAF1 partially rescued FBXL19-AS1 knockdown-mediated inhibition of angiogenesis and progression in lung cancer. Together, these results indicated that FBXL19-AS1 was involved in progression and angiogenesis in lung cancer by targeting miR-431-5p/RAF1 axis, which provided a new insight into the therapeutic strategies of lung cancer.

scholarly journals Sevoflurane inhibits proliferation, invasion, but enhances apoptosis of lung cancer cells by Wnt/β-catenin signaling via regulating lncRNA PCAT6/ miR-326 axis

2020 ◽  
Vol 15 (1) ◽  
pp. 159-172
Author(s):  
Guoning Su ◽  
Zhibing Yan ◽  
Min Deng
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Volatile Anesthetic ◽  
Lung Cancer Cells ◽  
Luciferase Reporter ◽  
Dependent Manner ◽  
Luciferase Reporter Gene ◽  
Western Blot Assay ◽  
Gene Assay ◽  
Cancer Tissues

AbstractSevoflurane was frequently used as a volatile anesthetic in cancer surgery. However, the potential mechanism of sevoflurane on lung cancer remains largely unclear. In this study, lung cancer cell lines (H446 and H1975) were treated by various concentrations of sevoflurane. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assessment and colony formation assay were performed to detect the cell viability and proliferation, separately. Also, transwell assay or flow cytometry assay was applied as well to evaluate the invasive ability or apoptosis in lung cancer cells, respectively. Western blot assay was employed to detect the protein levels of β-catenin and Wnt5a. Moreover, quantitative real-time polymerase chain reaction (qRT-PCR) was used to examine the expression level of prostate cancer-associated transcript 6 (PCAT6) and miR-326 in lung cancer tissues and cells. The target interaction between miR-326 and PCAT6 or Wnt5a was predicted by bioinformatics analysis and verified by the dual-luciferase reporter gene assay. Sevoflurane inhibited the abilities on viability, proliferation, invasion, and activation of Wnt/β-catenin signaling, but promoted apoptosis of H446 and H1975 cells in a dose-dependent manner. The expression of PCAT6 was increased in lung cancer tissues and cells, except for that of miR-326. Besides, sevoflurane could lead to expressed limitation of PCAT6 or improvement of miR-326. This process presented a stepwise manner. Up-regulation of PCAT6 restored the suppression of sevoflurane on abilities of proliferation, invasion, rather than apoptosis, and re-activated the Wnt5a/β-catenin signaling in cells. Moreover, the putative binding sites between miR-326 and PCTA6 or Wnt5a were predicted by starBase v2.0 software online. PCAT6 suppressing effects on cells could be reversed by pre-treatment with miR-326 vector. The promotion of Wnt5a inverted effects led from miR-326 or sevoflurane. Our study indicated that sevoflurane inhibited the proliferation, and invasion, but enhanced the apoptosis in lung cancer cells by regulating the lncRNA PCAT6/miR-326/Wnt5a/β-catenin axis.

scholarly journals POU2F2 promotes the proliferation and motility of lung cancer cells by activating AGO1

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ronggang Luo ◽  
Yi Zhuo ◽  
Quan Du ◽  
Rendong Xiao
Keyword(s):  
Lung Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Cancer Tissues

Abstract Background To detect and investigate the expression of POU domain class 2 transcription factor 2 (POU2F2) in human lung cancer tissues, its role in lung cancer progression, and the potential mechanisms. Methods Immunohistochemical (IHC) assays were conducted to assess the expression of POU2F2 in human lung cancer tissues. Immunoblot assays were performed to assess the expression levels of POU2F2 in human lung cancer tissues and cell lines. CCK-8, colony formation, and transwell-migration/invasion assays were conducted to detect the effects of POU2F2 and AGO1 on the proliferaion and motility of A549 and H1299 cells in vitro. CHIP and luciferase assays were performed for the mechanism study. A tumor xenotransplantation model was used to detect the effects of POU2F2 on tumor growth in vivo. Results We found POU2F2 was highly expressed in human lung cancer tissues and cell lines, and associated with the lung cancer patients’ prognosis and clinical features. POU2F2 promoted the proliferation, and motility of lung cancer cells via targeting AGO1 in vitro. Additionally, POU2F2 promoted tumor growth of lung cancer cells via AGO1 in vivo. Conclusion We found POU2F2 was highly expressed in lung cancer cells and confirmed the involvement of POU2F2 in lung cancer progression, and thought POU2F2 could act as a potential therapeutic target for lung cancer.

scholarly journals SUMO1 promotes the proliferation and invasion of non-small cell lung cancer cells by regulating NF-κB

2018 ◽  
Vol 10 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Changkang Ke ◽  
Kai Zhu ◽  
Ying Sun ◽  
Yunfeng Ni ◽  
Zhipei Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung ◽  
Proliferation And Invasion

scholarly journals Quiescin Sulfhydryl Oxidase 1 (QSOX1) Secreted by Lung Cancer Cells Promotes Cancer Metastasis

2018 ◽  
Vol 19 (10) ◽  
pp. 3213 ◽  
Author(s):  
Hye-Jin Sung ◽  
Jung-Mo Ahn ◽  
Yeon-Hee Yoon ◽  
Sang-Su Na ◽  
Young-Jin Choi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cancer Metastasis ◽  
Lung Cancer Cells ◽  
Migration And Invasion ◽  
Sulfhydryl Oxidase ◽  
Lung Cancers ◽  
Normal Tissues ◽  
Cancer Tissues ◽  
Quiescin Sulfhydryl Oxidase

As lung cancer shows the highest mortality in cancer-related death, serum biomarkers are demanded for lung cancer diagnosis and its treatment. To discover lung cancer protein biomarkers, secreted proteins from primary cultured lung cancer and adjacent normal tissues from patients were subjected to LC/MS–MS proteomic analysis. Quiescin sulfhydryl oxidase (QSOX1) was selected as a biomarker candidate from the enriched proteins in the secretion of lung cancer cells. QSOX1 levels were higher in 82% (51 of 62 tissues) of lung cancer tissues compared to adjacent normal tissues. Importantly, QSOX1 serum levels were significantly higher in cancer patients (p < 0.05, Area Under curve (AUC) = 0.89) when measured by multiple reaction monitoring (MRM). Higher levels of QSOX1 were also uniquely detected in lung cancer tissues, among several other solid cancers, by immunohistochemistry. QSOX1-knock-downed Lewis lung cancer (LLC) cells were less viable from oxidative stress and reduced migration and invasion. In addition, LLC mouse models with QSOX1 knock-down also proved that QSOX1 functions in promoting cancer metastasis. In conclusion, QSOX1 might be a lung cancer tissue-derived biomarker and be involved in the promotion of lung cancers, and thus can be a therapeutic target for lung cancers.

scholarly journals Histone deacetylase�5 promotes the proliferation and invasion of lung cancer cells

2018 ◽  
Author(s):  
Lou Zhong ◽  
Siyuan Sun ◽  
Sumei Yao ◽  
Xiao Han ◽  
Mingming Gu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Histone Deacetylase ◽  
Lung Cancer Cells ◽  
Proliferation And Invasion

scholarly journals Rhophilin-2 Upregulates Glutamine Synthetase by Stabilizing c-Myc Protein and Confers Resistance to Glutamine Deprivation in Lung Cancer

2021 ◽  
Vol 10 ◽  
Author(s):  
Dakai Xiao ◽  
Jiaxi He ◽  
Zhihua Guo ◽  
Huiming He ◽  
Shengli Yang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Glutamine Synthetase ◽  
Lung Adenocarcinoma ◽  
Cancer Cells ◽  
Clinical Sample ◽  
Glutamine Metabolism ◽  
Lung Cancer Cells ◽  
Mesenchymal Transformation ◽  
Proliferation And Invasion

IntroductionRHPN2, a member of rhophilin family of rho-binding proteins, regulates actin cytoskeleton and vesicular trafficking, and promotes mesenchymal transformation in cancer. We have found that RHPN2 was significantly mutated in lung adenocarcinoma (LUAD). However, the role of RHPN2 in lung cancer is not fully understood.MethodsIn the present study, we investigated the expression of RHPN2 in 125 patients with LUAD by qRT-PCR and correlated its expression with clinical characteristics. The effects of RHPN2 on the proliferation and invasion of lung cancer cells were determined by CCK-8 and in vitro transwell assays, clonogenic assay, and xenograft mouse model. The RhoA pull down assay and Western blotting were performed to elucidate the mechanism of RNPN2 in tumorigenesis of lung cancer.ResultsRHPN2 was overexpressed in tumors from LUAD, and high levels of RHPN2 were associated with poor prognosis of LUAD patients. RHPN2 was required for proliferation and invasion of lung cancer cells. Intriguingly, overexpression of RHPN2 conferred the resistance to glutamine depletion in lung cancer cells. Mechanistic studies revealed that ectopic overexpression of RHPN2 promoted the stability of c-Myc protein via phosphorylation at Ser62 and increased c-Myc target glutamine synthetase (GS). Analysis of GS expression in clinical sample showed that the expression of GS was elevated in tumor cells. Kaplan-Meier analysis revealed that high levels of GS were significantly associated with worse overall survival time of the patients with LUAD.ConclusionsTaken together, this study suggested that RHPN2 was involved in tumorigenesis of lung cancer via modulating c-Myc stability and the expression of its target GS in lung adenocarcinoma, which links RHPN2 and glutamine metabolism.

scholarly journals Loss of RASSF2 Enhances Tumorigencity of Lung Cancer Cells and Confers Resistance to Chemotherapy

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Jennifer Clark ◽  
Jessica Freeman ◽  
Howard Donninger
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Morphological Changes ◽  
Lung Cancer Cells ◽  
Ras Signaling ◽  
Independent Manner ◽  
Primary Tumors ◽  
Bona Fide ◽  
Proliferation And Invasion ◽  
Resistance To Chemotherapy

RASSF2 is a novel pro-apoptotic effector of K-Ras that is frequently inactivated in a variety of primary tumors by promoter methylation. Inactivation of RASSF2 enhances K-Ras-mediated transformation and overexpression of RASSF2 suppresses tumor cell growth. In this study, we confirm that RASSF2 and K-Ras form an endogenous complex, validating that RASSF2 is a bona fide K-Ras effector. We adopted an RNAi approach to determine the effects of inactivation of RASSF2 on the transformed phenotype of lung cancer cells containing an oncogenic K-Ras. Loss of RASSF2 expression resulted in a more aggressive phenotype that was characterized by enhanced cell proliferation and invasion, decreased cell adhesion, the ability to grow in an anchorage-independent manner and cell morphological changes. This enhanced transformed phenotype of the cells correlated with increased levels of activated AKT, indicating that RASSF2 can modulate Ras signaling pathways. Loss of RASSF2 expression also confers resistance to taxol and cisplatin, two frontline therapeutics for the treatment of lung cancer. Thus we have shown that inactivation of RASSF2, a process that occurs frequently in primary tumors, enhances the transforming potential of activated K-Ras and our data suggests that RASSF2 may be a novel candidate for epigenetic-based therapy in lung cancer.

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