Salinomycin can effectively kill ALDHhigh stem-like cells on gastric cancer

Zhi, Qiao Ming; Chen, Xue Hua; Ji, Jun; Zhang, Jia Nian; Li, Jian Fang; Cai, Qing; Liu, Bingya; Gu, Qin; Zhu, Zheng; Yu, Ying

doi:10.1016/j.biopha.2011.06.006

Cited by 98 publications

(74 citation statements)

References 31 publications

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“…However, the fall in autophagy flux was greater in ALDH + population than in the ALDH − one (51% vs. 10%, respectively). Consistent with data showing that Sal can effectively kills ALDH + gastric cells, 64 we also observed that apoptotic cell death was higher in the ALDH1 + population derived from the HMLER cell line than in the ALDH − population. These findings are consistent with data indicating that Sal-induced apoptosis is increased in autophagy-deficient cells.…”

Section: Discussionsupporting

confidence: 80%

Inhibition of the autophagic flux by salinomycin in breast cancer stem-like/progenitor cells interferes with their maintenance

et al. 2013

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Section: Discussionsupporting

confidence: 80%

Inhibition of the autophagic flux by salinomycin in breast cancer stem-like/progenitor cells interferes with their maintenance

et al. 2013

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“…Moreover, high ALDH1A expression has been associated with adverse prognosis in breast, lung, serous ovarian, pancreatic, bladder, prostate and oesophageal cancer [76]. With regard to GC, the findings are still conflicting and inconclusive [77][78][79][80][81][82][83] and, to our knowledge, no previous studies have investigated ALDH1A expression in HDGC and its precursor lesions, to assess the validity of this putative CSC biomarker in this specific setting.…”

Section: New Insights In Morphological Immunohistochemical and Genetmentioning

confidence: 99%

Histopathological, Molecular, and Genetic Profile of Hereditary Diffuse Gastric Cancer: Current Knowledge and Challenges for the Future

Post

Gullo

Oliveira

et al. 2016

Advances in Experimental Medicine and Biology

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Familial clustering is seen in 10% of gastric cancer cases and approximately 1-3% of gastric cancer arises in the setting of hereditary diffuse gastric cancer (HDGC). In families with HDGC, gastric cancer presents at young age. HDGC is predominantly caused by germline mutations in CDH1 and in a minority by mutations in other genes, including CTNNA1. Early stage HDGC is characterized by a few, up to dozens of intramucosal foci of signet ring cell carcinoma and its precursor lesions. These include in situ signet ring cell carcinoma and pagetoid spread of signet ring cells. Advanced HDGC presents as poorly cohesive/diffuse type carcinoma, normally with very few typical signet ring cells, and has a poor prognosis.Currently, it is unknown which factors drive the progression towards aggressive disease, but it is clear that most intramucosal lesions will not have such progression.Immunohistochemical profile of early and advanced HDGC is often characterised by abnormal E-cadherin immunoexpression, including absent or reduced membranous expression, as well as "dotted" or cytoplasmic expression. However, membranous expression of E-cadherin does not exclude HDGC. Intramucosal HDGC (pT1a) presents with an "indolent" phenotype, characterized by typical signet ring cells without immunoexpression of Ki-67 and p53, while advanced carcinomas (pT>1) display an "aggressive" phenotype with pleomorphic cells, that are immunoreactive for Ki-67 and p53. These features show that the IHC profile is different between intramucosal and more advanced HDGC, providing evidence of phenotypic heterogeneity, and may help to define predictive biomarkers of progression from indolent to aggressive, widely invasive carcinomas.6

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“…They found that the proliferation rate of GCSC was dramatically inhibited by knockdown of Wnt-1. Also, Salinomycin, an antibiotic thought to suppress Wnt/b-catenin signal transduction can inhibit GCSC [47,194] . Finally, the importance of the Wnt/b-catenin pathway for the selfrenewal of CSCs in human gastric cancer have also been suggested by proving that stimulation with Dkk-1 could decrease the self-renewal ability of cancer stemlike cells [46] .…”

Section: Wnt/b-catenin Signaling In the Gastric Cancer Stem Cellsmentioning

confidence: 99%

Role of the Wnt/β-catenin pathway in gastric cancer: An in-depth literature review

Chiurillo

2015

WJEM

262

219

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Gastric cancer remains one of the most common cancers worldwide and one of the leading cause for cancerrelated deaths. Gastric adenocarcinoma is a multifactorial disease that is genetically, cytologically and architecturally more heterogeneous than other gastrointestinal carcinomas. The identification of specific membrane, intracellular, and extracellular components of the Wnt pathway has revealed potential targets for gastric cancer therapy. High-throughput "omics" approaches will help in the search for Wnt pathway antagonist in the near future.

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Salinomycin can effectively kill ALDHhigh stem-like cells on gastric cancer

Cited by 98 publications

References 31 publications

Inhibition of the autophagic flux by salinomycin in breast cancer stem-like/progenitor cells interferes with their maintenance

Inhibition of the autophagic flux by salinomycin in breast cancer stem-like/progenitor cells interferes with their maintenance

Histopathological, Molecular, and Genetic Profile of Hereditary Diffuse Gastric Cancer: Current Knowledge and Challenges for the Future

Role of the Wnt/β-catenin pathway in gastric cancer: An in-depth literature review

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