scholarly journals The critical role of HDAC1 activates NSCLC growth by nicotine resistance Cisplatin

2020 ◽  
Author(s):  
Ching-Yi Peng ◽  
Jia-Ping Wu
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Growth ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cisplatin Resistance ◽  
Critical Role ◽  
Cancer Cell Growth ◽  
Histone Deacetylase 1

AbstractNicotine is active in highly cisplatin-resistant cancer cells; however, there is little evidence for its resistant activity in lung cancer with cisplatin. Many mechanisms of cisplatin resistance have been proposed. The mechanisms of the nicotine treatment of cisplatin-resistant lung cancer for histone deacetylase 1 (HDAC1) activity is unknown. Nicotine was used to analyze cisplatin-resistant non-small cell lung cancer (NSCLC) cancer cell growth. Western blot was used to analyze cell cycle-related proteins. Cancer cell viability (cell survival) was measured with MTT assay. HDAC1 transfected NSCLC cells were used to analyze the direct binding between cytosol and nucleus distribution. Here, using cell viability and migration methods we firstly found nicotine regulated cisplatin-resistant NSCLC cells growth by targeting HDAC1. Expression of cisplatin was negatively correlated with HDAC1. And HDAC1 inhibitor, VPA, in the NSCLC cancer cells were predicted. Further experiments confirmed that HDAC1 directly targeted E2F and cisplatin. Besides, HDAC1 and cisplatin inhibited NSCLC cell growth and reduced expression of E2F and Cyclin E proteins. The use of nicotine compromised cisplatin-induced E2F suppression and cancer cell growth. NSCLC cancer cells co-transfected with nicotine and HDAC1 had a higher cell cycle proliferation. Taken all together, cisplatin interferes with DNA replication kills the cancer cell fastest proliferation; however, nicotine increased detoxification of cisplatin, inhibition of apoptosis and DNA repair, induced cisplatin resistance.

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

scholarly journals Atypical Protein Kinase Cι Plays a Critical Role in Human Lung Cancer Cell Growth and Tumorigenicity

2005 ◽  
Vol 280 (35) ◽  
pp. 31109-31115 ◽  
Author(s):  
Roderick P. Regala ◽  
Capella Weems ◽  
Lee Jamieson ◽  
John A. Copland ◽  
E. Aubrey Thompson ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Protein Kinase ◽  
Cell Growth ◽  
Cancer Cell ◽  
Human Lung ◽  
Critical Role ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
Human Lung Cancer Cell

LY294002 and Metformin Cooperatively Enhance the Inhibition of Growth and the Induction of Apoptosis of Ovarian Cancer Cells

2012 ◽  
Vol 22 (1) ◽  
pp. 15-22 ◽  
Author(s):  
Cuilan Li ◽  
Vincent Wing Sun Liu ◽  
David Wai Chan ◽  
Kwok Ming Yao ◽  
Hextan Yuen Sheung Ngan
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Flow Cytometry ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Mtor Pathway ◽  
Ovarian Cancer Cells ◽  
Cancer Cell Growth

BackgroundThe phosphoinositide 3 kinase (PI3K)/v-akt murine thymoma viral oncogene homolog (AKT)/mammalian target of rapamycin (mTOR) pathway is frequently aberrantly activated in ovarian cancer and confers the chemoresistant phenotype of ovarian cancer cells. LY294002 (PI3K inhibitor) and metformin (5′-adenosine monophosphate [AMP]-activated protein kinase [AMPK] activator) are 2 drugs that were known to inhibit mTOR expression through the AKT-dependent and AKT-independent pathways, respectively. In this study, we explored the effectiveness of LY294002 and metformin in combination on inhibition of ovarian cancer cell growth.MethodsWestern blotting was used to detect the changes of PI3K/AKT/mTOR and AMPK/acetyl-CoA carboxylase (ACC) signaling activities, cell cycle control, and apoptosis. Cell growth was evaluated by cell proliferation, colony formation, and soft agar assays. Flow cytometry was used to study cell cycle distribution and cell death upon drug treatment.ResultsOur study showed that LY294002 and metformin in combination could simultaneously enhance the repression of the PI3K/AKT/mTOR pathway and the activation of the AMPK/ACC pathway. The downstream target of AKT and AMPK, mTOR, was cooperatively repressed when the drugs were used together. The cell cycle regulatory factors, p53, p27, and p21, were up-regulated. On the other hand, caspase 3 and poly (ADP-ribose) polymerase activities involved in apoptosis were also activated. Cell growth assays indicated that LY294002 and metformin could effectively inhibit ovarian cancer cell growth. Flow cytometry analysis showed that the treatment of the 2 drugs mentioned above induced cell cycle arrest at G1 phase and increased sub-G1 apoptotic cells.ConclusionThe combinational use of LY294002 and metformin can enhance inhibition of the growth and induction of the apoptosis of ovarian cancer cells. Our results may provide significant insight into the future therapeutic regimens in ovarian cancer.

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 A Novel Muscarinic Antagonist R2HBJJ Inhibits Non-Small Cell Lung Cancer Cell Growth and Arrests the Cell Cycle in G0/G1

PLoS ONE ◽  
2012 ◽  
Vol 7 (12) ◽  
pp. e53170 ◽  
Author(s):  
Nan Hua ◽  
Xiaoli Wei ◽  
Xiaoyan Liu ◽  
Xiaoyun Ma ◽  
Xinhua He ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Growth ◽  
Small Cell Lung Cancer ◽  
Cancer Cell ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cell ◽  
Small Cell Lung ◽  
Cancer Cell Growth

scholarly journals 5-Demethyltangeretin inhibits human nonsmall cell lung cancer cell growth by inducing G2/M cell cycle arrest and apoptosis

2013 ◽  
Vol 57 (12) ◽  
pp. 2103-2111 ◽  
Author(s):  
Noppawat Charoensinphon ◽  
Peiju Qiu ◽  
Ping Dong ◽  
Jinkai Zheng ◽  
Pearline Ngauv ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Growth ◽  
Cell Cycle Arrest ◽  
Cancer Cell ◽  
Nonsmall Cell Lung Cancer ◽  
Lung Cancer Cell ◽  
M Cell ◽  
Cancer Cell Growth ◽  
Cycle Arrest

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.

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