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AMPK AND cancer

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https://www.readbyqxmd.com/read/28106780/integrins-and-cell-metabolism-an-intimate-relationship-impacting-cancer
#1
REVIEW
Rehman Ata, Costin N Antonescu
Integrins are important regulators of cell survival, proliferation, adhesion and migration. Once activated, integrins establish a regulated link between the extracellular matrix and the cytoskeleton. Integrins have well-established functions in cancer, such as in controlling cell survival by engagement of many specific intracellular signaling pathways and in facilitating metastasis. Integrins and associated proteins are regulated by control of transcription, membrane traffic, and degradation, as well as by a number of post-translational modifications including glycosylation, allowing integrin function to be modulated to conform to various cellular needs and environmental conditions...
January 18, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28103582/ampk-autophagy-inhibition-sensitizes-icaritin-induced-anti-colorectal-cancer-cell-activity
#2
Chunxian Zhou, Jun Gu, Gang Zhang, Da Dong, Qunying Yang, Min-Bin Chen, Dongfeng Xu
The current research studied the potential effect of autophagy on icaritin-induced anti-colorectal cancer (CRC) cell activity. Treatment of icaritin in both primary and established (HT-29) CRC cells induced feedback activation of autophagy, evidenced by p62 degradation, Beclin-1 and autophagy-related gene-5 (ATG-5) upregulation, as well as light chain 3B (LC3B)-GFP puncta formation. Pharmacological inhibiting of autophagy dramatically potentiated icaritin-induced CRC cell death and apoptosis. Meanwhile, shRNA-mediated knockdown of Beclin-1 or ATG-5 also sensitized icaritin-induced CRC cell death and apoptosis...
January 18, 2017: Oncotarget
https://www.readbyqxmd.com/read/28099841/targeted-inhibition-of-egfr-and-glutaminase-induces-metabolic-crisis-in-egfr-mutant-lung-cancer
#3
Milica Momcilovic, Sean T Bailey, Jason T Lee, Michael C Fishbein, Clara Magyar, Daniel Braas, Thomas Graeber, Nicholas J Jackson, Johannes Czernin, Ethan Emberley, Matthew Gross, Julie Janes, Andy Mackinnon, Alison Pan, Mirna Rodriguez, Melissa Works, Winter Zhang, Francesco Parlati, Susan Demo, Edward Garon, Kostyantyn Krysan, Tonya C Walser, Steven M Dubinett, Saman Sadeghi, Heather R Christofk, David B Shackelford
Cancer cells exhibit increased use of nutrients, including glucose and glutamine, to support the bioenergetic and biosynthetic demands of proliferation. We tested the small-molecule inhibitor of glutaminase CB-839 in combination with erlotinib on epidermal growth factor receptor (EGFR) mutant non-small cell lung cancer (NSCLC) as a therapeutic strategy to simultaneously impair cancer glucose and glutamine utilization and thereby suppress tumor growth. Here, we show that CB-839 cooperates with erlotinib to drive energetic stress and activate the AMP-activated protein kinase (AMPK) pathway in EGFR (del19) lung tumors...
January 17, 2017: Cell Reports
https://www.readbyqxmd.com/read/28099419/genomic-deletion-of-malic-enzyme-2-confers-collateral-lethality-in-pancreatic-cancer
#4
Prasenjit Dey, Joelle Baddour, Florian Muller, Chia Chin Wu, Huamin Wang, Wen-Ting Liao, Zangdao Lan, Alina Chen, Tony Gutschner, Yaan Kang, Jason Fleming, Nikunj Satani, Di Zhao, Abhinav Achreja, Lifeng Yang, Jiyoon Lee, Edward Chang, Giannicola Genovese, Andrea Viale, Haoqiang Ying, Giulio Draetta, Anirban Maitra, Y Alan Wang, Deepak Nagrath, Ronald A DePinho
The genome of pancreatic ductal adenocarcinoma (PDAC) frequently contains deletions of tumour suppressor gene loci, most notably SMAD4, which is homozygously deleted in nearly one-third of cases. As loss of neighbouring housekeeping genes can confer collateral lethality, we sought to determine whether loss of the metabolic gene malic enzyme 2 (ME2) in the SMAD4 locus would create cancer-specific metabolic vulnerability upon targeting of its paralogous isoform ME3. The mitochondrial malic enzymes (ME2 and ME3) are oxidative decarboxylases that catalyse the conversion of malate to pyruvate and are essential for NADPH regeneration and reactive oxygen species homeostasis...
January 18, 2017: Nature
https://www.readbyqxmd.com/read/28096382/mitochondrial-activation-chemicals-synergize-with-surface-receptor-pd-1-blockade-for-t-cell-dependent-antitumor-activity
#5
Kenji Chamoto, Partha S Chowdhury, Alok Kumar, Kazuhiro Sonomura, Fumihiko Matsuda, Sidonia Fagarasan, Tasuku Honjo
Although immunotherapy by PD-1 blockade has dramatically improved the survival rate of cancer patients, further improvement in efficacy is required to reduce the fraction of less sensitive patients. In mouse models of PD-1 blockade therapy, we found that tumor-reactive cytotoxic T lymphocytes (CTLs) in draining lymph nodes (DLNs) carry increased mitochondrial mass and more reactive oxygen species (ROS). We show that ROS generation by ROS precursors or indirectly by mitochondrial uncouplers synergized the tumoricidal activity of PD-1 blockade by expansion of effector/memory CTLs in DLNs and within the tumor...
January 17, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28069379/ndrg2-overexpression-suppresses-hepatoma-cells-survival-during-metabolic-stress-through-disturbing-the-activation-of-fatty-acid-oxidation
#6
Tao Pan, Mei Zhang, Fang Zhang, Guang Yan, Yi Ru, Qinhao Wang, Yao Zhang, Xuehui Wei, Xinyuan Xu, Lan Shen, Jian Zhang, Kaichun Wu, Libo Yao, Xia Li
Because of the high nutrient consumption and inadequate vascularization, solid tumor constantly undergoes metabolic stress during tumor development. Oncogenes and tumor suppressor genes participated in cancer cells' metabolic reprogramming. N-Myc downstream regulated gene 2 (NDRG2) is a recently identified tumor suppressor gene, but its function in cancer metabolism, particularly during metabolic stress, remains unclear. In this study, we found that NDRG2 overexpression significantly reduced hepatoma cell proliferation and enhanced cell apoptosis under glucose limitation...
January 6, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28066797/mitochondrial-dysfunction-activates-the-ampk-signaling-and-autophagy-to-promote-cell-survival
#7
Baozhong Zhao, Lei Qiang, Joy Joseph, Balaraman Kalyanaraman, Benoit Viollet, Yu-Ying He
Autophagy is a cellular self-eating process essential for stress response and maintaining tissue homeostasis by lysosomal degradation of unwanted or damaged proteins and organelles. Here, we show that cells with defective mitochondria induce autophagy to promote cell survival through activating the AMPK pathway. Loss of mitochondrial complex III protein cytochrome b activates the AMPK signaling and induced autophagy. Inhibiting mitochondria energetics by mitochondria-targeted agents activates the AMPK signaling and induced autophagy...
March 2016: Genes & Diseases
https://www.readbyqxmd.com/read/28061838/cryptotanshinone-activates-ampk-tsc2-axis-leading-to-inhibition-of-mtorc1-signaling-in-cancer-cells
#8
Wenxing Chen, Yanhong Pan, Siliang Wang, Yuping Liu, Guangying Chen, Liang Zhou, Wenting Ni, Aiyun Wang, Yin Lu
BACKGROUND: Cryptotanshinone (CPT), a fat-soluble phenanthraquinone from Salvia miltiorrhiza Bunge, has been demonstrated to inhibit phosphorylation of p70 S6 kinase 1 (S6K1) and eukaryotic initiation factor 4E binding protein 1 (4E-BP1), a couple of direct downstream effectors of the mammalian target of rapamycin complex 1 (mTORC1), resulting in cancer cell arrested in G0 phase and subsequent inhibition of proliferation. However, its concrete molecular mechanism about how CPT inhibits mTORC1 signaling pathway is unclear...
January 7, 2017: BMC Cancer
https://www.readbyqxmd.com/read/28052040/nuclear-receptor-retinoid-related-orphan-receptor-alpha-promotes-apoptosis-but-is-reduced-in-human-gastric-cancer
#9
Zhengguang Wang, Fangyuan Xiong, Xiaoshan Wang, Yijun Qi, Haoyuan Yu, Yong Zhu, Huaqing Zhu
Retinoid-related orphan receptor α (RORα) is a nuclear receptor, which regulates inflammation and immune responses, lipid metabolism and circadian rhythm. Although RORα suppresses breast tumor invasion, it is unknown whether RORα is dysregulated in gastric cancer leading to cellular survival. Therefore, we hypothesize that RORα is dysfunctional in gastric carcinoma and this causes decreased apoptosis in gastric cancer cells. To test this hypothesis, we employed human gastric cancer tissues with different stages to determine RORα expression, as well as in vitro human gastric cancer cells to determine how RORα is reduced during apoptosis...
December 29, 2016: Oncotarget
https://www.readbyqxmd.com/read/28052030/the-angiotensin-ii-type-1-receptor-antagonist-telmisartan-inhibits-cell-proliferation-and-tumor-growth-of-esophageal-adenocarcinoma-via-the-ampk%C3%AE-mtor-pathway-in-vitro-and-in-vivo
#10
Shintaro Fujihara, Asahiro Morishita, Kana Ogawa, Tomoko Tadokoro, Taiga Chiyo, Kiyohito Kato, Hideki Kobara, Hirohito Mori, Hisakazu Iwama, Tsutomu Masaki
Telmisartan, a widely used antihypertensive drug, is an angiotensin II type 1 (AT1) receptor blocker (ARB). This drug inhibits cancer cell proliferation, but the underlying mechanisms in various cancers, including esophageal cancer, remain unknown. The aim of the present study was to evaluate the effects of telmisartan on human esophageal cancer cell proliferation in vitro and in vivo. We assessed the effects of telmisartan on human esophageal adenocarcinoma (EAC) cells using the cell lines OE19, OE33, and SKGT-4...
December 28, 2016: Oncotarget
https://www.readbyqxmd.com/read/28035400/ampk-activators-suppress-breast-cancer-cell-growth-by-inhibiting-dvl3-facilitated-wnt-%C3%AE-catenin-signaling-pathway-activity
#11
Yu-Feng Zou, Chun-Wei Xie, Shi-Xin Yang, Jian-Ping Xiong
Adenosine monophosphate-activated protein kinase (AMPK) is a principal regulator of metabolism and the conservation of energy in cells, and protects them from exposure to various stressors. AMPK activators may exhibit therapeutic potential as suppressors of cell growth; however, the molecular mechanism underlying this phenomenon in various cancer cells remains to be fully elucidated. The present study investigated the effects of AMPK activators on breast cancer cell growth and specified the underlying molecular mechanism...
February 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28034771/lkb1-promotes-metabolic-flexibility-in-response-to-energy-stress
#12
Seth J Parker, Robert U Svensson, Ajit S Divakaruni, Austin E Lefebvre, Anne N Murphy, Reuben J Shaw, Christian M Metallo
The Liver Kinase B1 (LKB1) tumor suppressor acts as a metabolic energy sensor to regulate AMP-activated protein kinase (AMPK) signaling and is commonly mutated in various cancers, including non-small cell lung cancer (NSCLC). Tumor cells deficient in LKB1 may be uniquely sensitized to metabolic stresses, which may offer a therapeutic window in oncology. To address this question we have explored how functional LKB1 impacts the metabolism of NSCLC cells using (13)C metabolic flux analysis. Isogenic NSCLC cells expressing functional LKB1 exhibited higher flux through oxidative mitochondrial pathways compared to those deficient in LKB1...
December 26, 2016: Metabolic Engineering
https://www.readbyqxmd.com/read/28031534/autophagy-inhibition-enhances-photocytotoxicity-of-photosan-ii-in-human-colorectal-cancer-cells
#13
Li Xiong, Zhipeng Liu, Guoqing Ouyang, Liangwu Lin, He Huang, Hongxiang Kang, Wei Chen, Xiongying Miao, Yu Wen
Photodynamic therapy (PDT) has emerged as an attractive therapeutic treatment for colorectal cancer because of its accessibility through endoscopy and its ability to selectively target tumors without destroying the anatomical integrity of the colon. We therefore investigated the therapeutic relevance of the interplay between autophagy and apoptosis in Photosan-II (PS-II)-mediated photodynamic therapy (PS-PDT) in in vitro and in vivo models for human colorectal cancer. We observed that PS-PDT-induced dose-dependently triggered apoptosis and autophagy in both SW620 and HCT116 cells...
December 23, 2016: Oncotarget
https://www.readbyqxmd.com/read/28011481/metformin-exerts-antiproliferative-and-anti-metastatic-effects-against-cholangiocarcinoma-cells-by-targeting-stat3-and-nf-%C3%A4-b
#14
Charupong Saengboonmee, Wunchana Seubwai, Ubon Cha'on, Kanlayanee Sawanyawisuth, Sopit Wongkham, Chaisiri Wongkham
BACKGROUND/AIM: Cholangiocarcinoma (CCA) is an aggressive cancer for which standard treatments are still ineffective. This study demonstrated the antiproliferative and anti-metastatic activity of metformin, an anti-diabetic drug, in CCA cells. MATERIALS AND METHODS: Cell proliferation, migration/invasion and anoikis resistance were determined. The underlying mechanisms were identified using western blotting and immunocytofluorescence. RESULTS: Metformin significantly suppressed proliferation of CCA cells in a dose- and time-dependent manner, regardless of glucose present in the medium...
January 2017: Anticancer Research
https://www.readbyqxmd.com/read/28003763/isoorientin-induces-apoptosis-decreases-invasiveness-and-downregulates-vegf-secretion-by-activating-ampk-signaling-in-pancreatic-cancer-cells
#15
Tingting Ye, Jiadong Su, Chaohao Huang, Dinglai Yu, Shengjie Dai, Xince Huang, Bicheng Chen, Mengtao Zhou
Isoorientin (or homoorientin) is a flavone, which is a chemical flavonoid-like compound, and a 6-C-glucoside of luteolin. Isoorientin has been demonstrated to have anti-cancer activities against various tumors, but its effects on pancreatic cancer (PC) have not been studied in detail. In this study, we aim to investigate whether isoorientin has potential anti-PC effects and its underlying mechanism. In PC, isoorientin strongly inhibited the survival of the cells, induced cell apoptosis, and decreased its malignancy by reversing the expression of epithelial-mesenchymal transition and matrix metalloproteinase and decreased vascular endothelial growth factor expression...
2016: OncoTargets and Therapy
https://www.readbyqxmd.com/read/27996156/%C3%AE-enolase-promotes-tumorigenesis-and-metastasis-via-regulating-ampk-mtor-pathway-in-colorectal-cancer
#16
Panpan Zhan, Shihu Zhao, Hua Yan, Chunli Yin, Yi Xiao, Yunshan Wang, Ruoxuan Ni, Weiwen Chen, Guangwei Wei, Pengju Zhang
BACKGROUND: α-enolase (ENO1) plays pivotal roles in several types of cancer, but its clinical significance, functional role and possible mechanism in colorectal cancer (CRC) have remained unclear. METHODS: Expression level of ENO1 in CRC tissues was examined by qRT-PCR, Western blot and immunohistochemistry. The effects of ENO1 on cell growth were investigated by MTT, colony formation, flow cytometry assays and in vivo tumorigenic capacity analysis. The impacts of ENO1 on cell migration and invasion were also explored by scratch-healing, Transwell or Matrigel chamber assays and in vivo metastatic capacity analysis...
December 20, 2016: Molecular Carcinogenesis
https://www.readbyqxmd.com/read/27989873/a-platycoside-rich-fraction-from-the-root-of-platycodon-grandiflorum-enhances-cell-death-in-a549-human-lung-carcinoma-cells-via-mainly-ampk-mtor-akt-signal-mediated-autophagy-induction
#17
Nam-Hui Yim, Youn-Hwan Hwang, Chun Liang, Jin Yeul Ma
ETHNOPHARMACOLOGICAL RELEVANCE: The root of Platycodon grandiflorum (PG), commonly known as Kilkyong in Korea, Jiegeng in China, and Kikyo in Japan, has been extensively used as a traditional anti-inflammatory medicine in Asia for the treatment of respiratory conditions, such as bronchitis, asthma, and tonsillitis. Platycosides isolated from PG are especially well-known for their anti-cancer effects. AIM OF THE STUDY: We investigated the involvement of autophagic cell death and other potential molecular mechanisms induced by the platycoside-containing butanol fraction of PG (PGB) in human lung carcinoma cells...
October 27, 2016: Journal of Ethnopharmacology
https://www.readbyqxmd.com/read/27951515/polyphenolics-from-mango-mangifera-indica-l-suppress-breast-cancer-ductal-carcinoma-in-situ-proliferation-through-activation-of-ampk-pathway-and-suppression-of-mtor-in-athymic-nude-mice
#18
Matthew J Nemec, Hyemee Kim, Alexandria B Marciante, Ryan C Barnes, Erik D Hendrick, William H Bisson, Stephen T Talcott, Susanne U Mertens-Talcott
The objective of this study was to assess the underlying mechanisms of mango polyphenol decreased cell proliferation and tumor volume in ductal carcinoma in situ breast cancer. We hypothesized that mango polyphenols suppress signaling along the AKT/mTOR axis while up-regulating AMPK. To test this hypothesis, mango polyphenols (0.8 mg gallic acid equivalents per day) and pyrogallol (0.2 mg/day) were administered for 4 weeks to mice xenografted with MCF10DCIS.com cells subcutaneously (n=10 per group). Tumor volumes were significantly decreased, both mango and pyrogallol groups displayed greater than 50% decreased volume compared to control...
November 15, 2016: Journal of Nutritional Biochemistry
https://www.readbyqxmd.com/read/27940576/aspirin-suppresses-growth-in-pi3k-mutant-breast-cancer-by-activating-ampk-and-inhibiting-mtorc1-signaling
#19
Whitney S Henry, Tyler Laszewski, Tiffany Tsang, Francisco Beca, Andrew H Beck, Sandra S McAllister, Alex Toker
Despite the high incidence of oncogenic mutations in PIK3CA, the gene encoding the catalytic subunit of phosphoinositide 3-kinase (PI3K), PI3K inhibitors have yielded little clinical benefit for breast cancer patients. Recent epidemiological studies have suggested a therapeutic benefit from aspirin intake in cancers harboring oncogenic PIK3CA. Here we show that mutant PIK3CA-expressing breast cancer cells have greater sensitivity to aspirin-mediated growth suppression than their wild-type counterparts. Aspirin decreased viability and anchorage-independent growth of mutant PIK3CA breast cancer cells independently of its effects on cyclooxygenase-2 (COX-2) and nuclear factor-kappa B (NF-κB)...
December 9, 2016: Cancer Research
https://www.readbyqxmd.com/read/27938509/sorafenib-and-2-deoxyglucose-synergistically-inhibit-proliferation-of-both-sorafenib-sensitive-and-resistant-hcc-cells-by-inhibiting-atp-production
#20
Ryan Reyes, Nissar Wani, Kalpana Ghoshal, Samson Jacob, Tasneem Motiwala
Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths globally. Sorafenib is the only first-line systemic drug for advanced HCC, but it has very limited survival benefits because patients treated with sorafenib either suffer from side effects or show disease progression after initial response. Thus, there is an urgent need to develop novel strategies for first-line and second-line therapy. The association between sorafenib resistance and glycolysis prompted us to screen several drugs with known anti-glycolytic activity to identify those that will sensitize cells to sorafenib...
16, 2016: Gene Expression
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