scholarly journals Glutamate-ammonia ligase promotes lung cancer cell growth through an enzyme-independent upregulation of CaMK2G under a glutamine-sufficient condition

2019 ◽  
Author(s):  
Jiangsha Zhao ◽  
Xiankun Zeng ◽  
Steven X. Hou
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Lung Cancer Cells ◽  
Sufficient Condition ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
Calcium Calmodulin Dependent ◽  
Survival And Growth

SUMMARYGlutamate-ammonia ligase (GLUL) is highly expressed in many cancer cells. Synthesizing glutamine by its enzyme function has been found to be important for supporting cancer cell survival and growth under glutamine restriction. However, GLUL’s functions under a glutamine-sufficient condition still have not been uncovered. Here we find that GLUL is highly expressed in lung cancer cells and provides survival and growth advantages under both glutamine restriction and adequacy conditions. Knocking down GLUL can block lung cancer cell growth in an enzyme-independent way when glutamine is sufficient. Mechanistically, GLUL regulates Calcium/Calmodulin Dependent Protein Kinase II Gamma (CaMK2G) expression at the transcription level, and CaMK2G is a major mediator in controlling cell growth under GLUL. The transcriptional regulation of CaMK2G is partially mediated by SMAD4. Our data unveil a new enzyme-independent function of GLUL in lung cancer cells under a glutamine-sufficient condition.

scholarly journals Beclin1-induced Autophagy Abrogates Radioresistance of Lung Cancer Cells by Suppressing Osteopontin

2012 ◽  
Vol 53 (3) ◽  
pp. 422-432 ◽  
Author(s):  
Seung-Hee Chang ◽  
Arash Minai-Tehrani ◽  
Ji-Young Shin ◽  
Sungjin Park ◽  
Ji-Eun Kim ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
Human Lung Cancer Cells

Abstract Osteopontin (OPN) serves as an indicator of resistance to radiotherapy. However, the role of OPN in the development of acquired radioresistance in human lung cancer cells has not yet been fully elucidated. Therefore, the potential importance of OPN as a marker of lung cancer with a potential significant role in the development of radioresistance against repeated radiotherapy has prompted us to define the pathways by which OPN regulates lung cancer cell growth. In addition, autophagy has been reported to play a key role in the radiosensitization of cancer cells. Here, we report that increased OPN expression through induction of nuclear p53 following irradiation was inhibited by exogenous beclin-1 (BECN1). Our results clearly show that BECN1 gene expression led to induction of autophagy and inhibition of cancer cell growth and angiogenesis. Our results suggest that the induction of autophagy abrogated the radioresistance of the cancer cells. Interestingly, we showed that knockdown of OPN by lentivirus-mediated shRNA induced the autophagy of human lung cancer cell. Taken together, these results suggest that OPN and BECN1 can be molecular targets for overcoming radioresistance by controlling autophagy.

scholarly journals Novel 2-step synthetic indole compound 1,1,3-tri(3-indolyl)cyclohexane inhibits cancer cell growth in lung cancer cells and xenograft models

Cancer ◽  
2008 ◽  
Vol 113 (4) ◽  
pp. 815-825 ◽  
Author(s):  
Ching-Hsiao Lee ◽  
Ching-Fa Yao ◽  
Sin-Ming Huang ◽  
Shengkai Ko ◽  
Yi-Hung Tan ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Lung Cancer Cells ◽  
Cancer Cell Growth ◽  
Indole Compound ◽  
Xenograft Models

A synthesized butyrolactone derivative in combination with chloroquine can inhibit cancer cell growth and lysosome vacuolation induced by chloroquine in A549 lung cancer cells

RSC Advances ◽  
2016 ◽  
Vol 6 (59) ◽  
pp. 54099-54101
Author(s):  
Xin-Peng Chen ◽  
Chuan-Dong Fan ◽  
Le Su ◽  
Bao-Xiang Zhao ◽  
Jun-Ying Miao
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Atpase Activity ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Lung Cancer Cells ◽  
Cancer Cell Growth ◽  
Non Coding Rna ◽  
A549 Lung

3BDO in combination with chloroquine could elevate the Na+,K+-ATPase activity and decrease the expression of competing endogenous non-coding RNA TGFB2-OT1. Therefore, ​ the combination inhibited the cells growth and lysosomal vacuolation induced by CQ.

ERGIC3 Silencing Additively Enhances the Growth Inhibition of BFA on Lung Adenocarcinoma Cells

2020 ◽  
Vol 20 (1) ◽  
pp. 67-75
Author(s):  
Qiurong Zhao ◽  
Mingsong Wu ◽  
Xiang Zheng ◽  
Lei Yang ◽  
Zhimin Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Endoplasmic Reticulum ◽  
Cell Growth ◽  
Lung Adenocarcinoma ◽  
Cancer Cells ◽  
Cancer Cell ◽  
A549 Cells ◽  
Golgi Body ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth

Background: Brefeldin A (BFA) has been known to induce endoplasmic reticulum stress (ERS) and Golgi body stress in cancer cells. ERGIC3 (endoplasmic reticulum-Golgi intermediate compartment 3) is a type II transmembrane protein located in the endoplasmic reticulum and Golgi body. ERGIC3 over-expression is frequently observed in cancer cells. Objective: In this study, we aim to explore whether BFA administered concurrently with ERGIC3 silencing would work additively or synergistically inhibit cancer cell growth. Methods: ERGIC3-siRNA was used to knock-down the expression of ERGIC3 and BFA was used to induce ERS in lung cancer cell lines GLC-82 and A549. Q-RT-PCR and Western Blot analysis were used to detect the expression of ERGIC3 and downstream molecules. GraphPad Prism 6 was used to quantify the data. Results: We demonstrated that silencing of ERGIC3 via siRNA effectively led to down-regulation of ERGIC3 at both mRNA and protein levels in GLC-82 and A549 cells. While BFA or ERGIC3- silencing alone could induce ERS and inhibit cell growth, the combination treatment of lung cancer cells with ERGIC3-silencing and BFA was able to additively enhance the inhibition effects of cell growth through up-regulation of GRP78 resulting in cell cycle arrest. Conclusion: ERGIC3 silencing in combination with BFA treatment could additively inhibit lung cancer cell growth. This finding might shed a light on new adjuvant therapy for lung adenocarcinoma.

USP10 inhibits lung cancer cell growth and invasion by upregulating PTEN

2017 ◽  
Vol 441 (1-2) ◽  
pp. 1-7 ◽  
Author(s):  
Jia Sun ◽  
Tianxiang Li ◽  
Yinying Zhao ◽  
Lirong Huang ◽  
Hua Sun ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth

scholarly journals Persistent effects of pair bonding in lung cancer cell growth in monogamous Peromyscus californicus

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Asieh Naderi ◽  
Elham Soltanmaohammadi ◽  
Vimala Kaza ◽  
Shayne Barlow ◽  
Ioulia Chatzistamou ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Nude Mice ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Peromyscus Californicus ◽  
Pair Bonds ◽  
The Impact

Epidemiological evidence suggests that social interactions and especially bonding between couples influence tumorigenesis, yet whether this is due to lifestyle changes, homogamy (likelihood of individuals to marry people of similar health), or directly associated with host-induced effects in tumors remains debatable. In the present study, we explored if tumorigenesis is associated with the bonding experience in monogamous rodents at which disruption of pair bonds is linked to anxiety and stress. Comparison of lung cancer cell spheroids that formed in the presence of sera from bonded and bond-disrupted deer mice showed that in monogamous Peromyscus polionotus and Peromyscus californicus, but not in polygamous Peromyscus maniculatus, the disruption of pair bonds altered the size and morphology of spheroids in a manner that is consistent with the acquisition of increased oncogenic potential. In vivo, consecutive transplantation of human lung cancer cells between P. californicus, differing in bonding experiences (n = 9 for bonded and n = 7 for bond-disrupted), and nude mice showed that bonding suppressed tumorigenicity in nude mice (p<0.05), suggesting that the protective effects of pair bonds persisted even after bonding ceased. Unsupervised hierarchical clustering indicated that the transcriptomes of lung cancer cells clustered according to the serum donors’ bonding history while differential gene expression analysis pointed to changes in cell adhesion and migration. The results highlight the pro-oncogenic effects of pair-bond disruption, point to the acquisition of expression signatures in cancer cells that are relevant to the bonding experiences of serum donors, and question the ability of conventional mouse models to capture the whole spectrum of the impact of the host in tumorigenesis.

scholarly journals FBXO22 mediates polyubiquitination and inactivation of LKB1 to promote lung cancer cell growth

2019 ◽  
Vol 10 (7) ◽  
Author(s):  
Xiao-Na Zhu ◽  
Ping He ◽  
Liang Zhang ◽  
Shuo Yang ◽  
Hui-Lin Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth

scholarly journals An Anti-Cancer Peptide LVTX-8 Inhibits the Proliferation and Migration of Lung Tumor Cells by Regulating Causal Genes’ Expression in p53-Related Pathways

Toxins ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 367
Author(s):  
Peng Zhang ◽  
Yujie Yan ◽  
Junting Wang ◽  
Xiaoping Dong ◽  
Gaihua Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
High Efficiency ◽  
Lung Tumor ◽  
Lung Cancer Cells ◽  
Helical Conformation ◽  
Anti Cancer ◽  
And Migration

Spider venom has been found to show its anticancer activity in a variety of human malignancies, including lung cancer. In this study, we investigated the anti-cancer peptide toxin LVTX-8, with linear amphipathic alpha-helical conformation, designed and synthesized from the cDNA library of spider Lycosa vittata. Multiple cellular methods, such as CCK-8 assay, flow cytometry, colony formation assay, Transwell invasion and migration assay, were performed to detect peptide-induced cell growth inhibition and anti-metastasis in lung cancer cells. Our results demonstrated that LVTX-8 displayed strong cytotoxicity and anti-metastasis towards lung cancer in vitro. Furthermore, LVTX-8 could suppress the growth and metastasis of lung cancer cells (A549 and H460) in nude mouse models. Transcriptomics, integrated with multiple bioinformatics analysis, suggested that the molecular basis of the LVTX-8-mediated inhibition of cancer cell growth and metastasis manifested in two aspects: Firstly, it could restrain the activity of cancer cell division and migration through the functional pathways, including “p53 hypoxia pathway” and “integrin signaling”. Secondly, it could regulate the expression level of apoptotic-related proteins, which may account for programmed apoptosis of cancer cells. Taken together, as an anticancer peptide with high efficiency and acceptable specificity, LVTX-8 may become a potential precursor of a therapeutic agent for lung cancer in the future.

Sign in / Sign up

Export Citation Format

Share Document