MiR-148a and miR-152 reduce tamoxifen resistance in ER+ breast cancer via downregulating ALCAM

Chen, Ming Jenn; Cheng, Ya Min; Chen, Chien‐Chung; Chen, Yu Chieh; Shen, Ching Ju

doi:10.1016/j.bbrc.2017.01.012

Cited by 47 publications

(36 citation statements)

References 23 publications

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“…5 as well as previously suggested 55 . Impaired ALCAM expression is associated with induced ER+ breast cancer cell apoptosis and autophagy 56 , and down-regulating ALCAM expression sensitizes ER+ breast cancers to Tamoxifen treatment 57 , suggesting the therapeutic potential of down-regulating ALCAM in ER+ cancers which is consistent with its relatively higher expression in such tumor subtypes (Fig. 7).…”

Section: Discussionmentioning

confidence: 61%

Integrated diagnostic network construction reveals a 4-gene panel and 5 cancer hallmarks driving breast cancer heterogeneity

Dai

Hua

Hong

2017

Sci Rep

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Breast cancer encompasses a group of heterogeneous diseases, each associated with distinct clinical implications. Dozens of molecular biomarkers capable of categorizing tumors into clinically relevant subgroups have been proposed which, though considerably contribute in precision medicine, complicate our understandings toward breast cancer subtyping and its clinical translation. To decipher the networking of markers with diagnostic roles on breast carcinomas, we constructed the diagnostic networks by incorporating 6 publically available gene expression datasets with protein interaction data retrieved from BioGRID on previously identified 1015 genes with breast cancer subtyping roles. The Greedy algorithm and mutual information were used to construct the integrated diagnostic network, resulting in 37 genes enclosing 43 interactions. Four genes, FAM134B, KIF2C, ALCAM, KIF1A, were identified having comparable subtyping efficacies with the initial 1015 genes evaluated by hierarchical clustering and cross validations that deploy support vector machine and k nearest neighbor algorithms. Pathway, Gene Ontology, and proliferation marker enrichment analyses collectively suggest 5 primary cancer hallmarks driving breast cancer differentiation, with those contributing to uncontrolled proliferation being the most prominent. Our results propose a 37-gene integrated diagnostic network implicating 5 cancer hallmarks that drives breast cancer heterogeneity and, in particular, a 4-gene panel with clinical diagnostic translation potential.

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Section: Discussionmentioning

confidence: 61%

Integrated diagnostic network construction reveals a 4-gene panel and 5 cancer hallmarks driving breast cancer heterogeneity

Dai

Hua

Hong

2017

Sci Rep

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“…At the same time an anticancer treatment like alitretinoin may exert a regulatory action on miR-375 expression in BC cells (195). miR-148a and miR-152 reduced tamoxifen resistance in ER+BC via direct down-regulating the activated leukocyte cell adhesion molecule (ALCAM) (429). miR-206 was elevated in ER+BC cell lines (161) and its knock-down induced resistance to tamoxifen, while its overexpression reduced it by regulating G1/S-related proteins (430).…”

Section: Drugs/non-coding Rnas Subnetworkmentioning

confidence: 99%

The Network of Non-coding RNAs in Cancer Drug Resistance

et al. 2018

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Non-coding RNAs (ncRNAs) have been implicated in most cellular functions. The disruption of their function through somatic mutations, genomic imprinting, transcriptional and post-transcriptional regulation, plays an ever-increasing role in cancer development. ncRNAs, including notorious microRNAs, have been thus proposed to function as tumor suppressors or oncogenes, often in a context-dependent fashion. In parallel, ncRNAs with altered expression in cancer have been reported to exert a key role in determining drug sensitivity or restoring drug responsiveness in resistant cells. Acquisition of resistance to anti-cancer drugs is a major hindrance to effective chemotherapy and is one of the most important causes of relapse and mortality in cancer patients. For these reasons, non-coding RNAs have become recent focuses as prognostic agents and modifiers of chemo-sensitivity. This review starts with a brief outline of the role of most studied non-coding RNAs in cancer and then highlights the modulation of cancer drug resistance via known ncRNAs based mechanisms. We identified from literature 388 ncRNA-drugs interactions and analyzed them using an unsupervised approach. Essentially, we performed a network analysis of the non-coding RNAs with direct relations with cancer drugs. Within such a machine-learning framework we detected the most representative ncRNAs-drug associations and groups. We finally discussed the higher integration of the drug-ncRNA clusters with the goal of disentangling effectors from downstream effects and further clarify the involvement of ncRNAs in the cellular mechanisms underlying resistance to cancer treatments.

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“…Previous studies have demonstrated that miR-152 acts as a tumor suppressor [21, 22, 24, 25]. However, the involvement of miR-152 in tumor immune is still poorly understood.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-152 regulates immune response via targeting B7-H1 in gastric carcinoma

Wang

Xie

et al. 2017

Oncotarget

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MiR-152 has been reported may be involved in carcinogenesis in gastric cancer. However, its role has not been comprehensively investigated in gastric cancer. We found miR-152 in human gastric cancer tissues were significantly lower than that in matched adjacent normal tissues. Meanwhile, lower miR-152 was also found in gastric cancer cell lines. The stage, tumor size and lymph node metastasis rate were significant higher in low–miR-152 group in clinical patients. Furthermore, there was a marked correlation between the levels of miR-152 and B7-H1 mRNA in gastric cancer tissues. Mechanistically, miR-152 directly bind to B7-H1 3′ untranslated region in gastric cancer cell and inhibited B7-H1 expression. Functional study demonstrated that elevation of miR-152 enhanced T cells proliferation and effector cytokines production via inhibiting B7-H1/PD-1 pathway. In conclusion, our work identified a novel mechanism by which immune response is increased by expression of miR-152 via targeting B7-H1. MiR-152 may be a potential therapeutic approach for gastric cancer.

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MiR-148a and miR-152 reduce tamoxifen resistance in ER+ breast cancer via downregulating ALCAM

Cited by 47 publications

References 23 publications

Integrated diagnostic network construction reveals a 4-gene panel and 5 cancer hallmarks driving breast cancer heterogeneity

Integrated diagnostic network construction reveals a 4-gene panel and 5 cancer hallmarks driving breast cancer heterogeneity

The Network of Non-coding RNAs in Cancer Drug Resistance

MicroRNA-152 regulates immune response via targeting B7-H1 in gastric carcinoma

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