Stress signaling and the shaping of the mammary tissue in development and cancer

Avivar-Valderas, Álvaro; Wen, Huei‐Chi; Aguirre‐Ghiso, Julio A.

doi:10.1038/onc.2013.554

Cited by 32 publications

(24 citation statements)

References 110 publications

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“…JNK and p38 have been shown to play important roles in mammary gland development [43]. Studies have shown that inactivation of p38 signaling and aberrant regulation of JNK foster breast cancer progression [44]…”

Section: Mitogen Activated Protein Kinases (Jnk P38)mentioning

confidence: 99%

Oxidative Stress and Carcinogenesis: Potential of Phytochemicals in Breast Cancer Therapy

Forcados

James

Sallau

et al. 2017

Nutrition and Cancer

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Breast cancer remains a burden in both developed and developing countries, with higher mortality in developing countries. Attempts to eradicate cancer have not been successful despite the progress made in the development of more novel chemotherapeutic drugs. Reactive-oxygen-species-mediated oxidative stress is known to play a role in breast cancer pathogenesis via genetic and epigenetic modifications, resulting in uncontrolled cell proliferation. Phytochemicals could provide leads for the development of alternative therapeutic agents due to their antioxidant activity, as well as their ability to induce apoptosis in cancer cells. However, most of the studies carried out using in vitro models do not continue with further studies in estrogen-receptor-positive in vivo breast cancer models, or fail to examine the possible biochemical mechanisms of phytochemical-based amelioration. This review examines oxidative-stress-mediated carcinogenesis and the potential of phytochemicals as anticancer agents.

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Section: Mitogen Activated Protein Kinases (Jnk P38)mentioning

confidence: 99%

Oxidative Stress and Carcinogenesis: Potential of Phytochemicals in Breast Cancer Therapy

Forcados

James

Sallau

et al. 2017

Nutrition and Cancer

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“…CSCs have been identified in lung cancer [7], breast cancer [8], glioblastoma [9], colorectal cancer [10], and HCC [11]. CSCs Xiaojun Yang, Jing Ye, and Han Yan contributed equally to this work.…”

Section: Introductionmentioning

confidence: 98%

MiR-491 attenuates cancer stem cells-like properties of hepatocellular carcinoma by inhibition of GIT-1/NF-κB-mediated EMT

Yang

Yan

et al. 2015

Tumor Biol.

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Hepatocellular carcinoma (HCC) is the most common liver malignancy. Current standard practices for treatment of HCC are less than satisfactory because of CSCs-mediated recurrence. For this reason, targeting CSCs, or cancer cells with CSCs-like properties, is a new approach for HCC treatment. As we reported previously, microRNA-491 (miR-491) is lower expressed in poorly differentiated HCC tissues relative to well-differentiated HCC tissues. Here, we further evaluate the effects of miR-491 on the CSCs-like properties by using HCC cell lines and HCC tissue samples. Our data showed that miR-491 had a negative relationship with CSCs-like properties both in cell lines and tissue samples of HCC. Further, miR-491 levels of non-recurrence HCC tissues were higher than those of recurrence HCC tissues. In HCC cell lines, nuclear factor kappa B (NF-κB)/snail pathway was involved in the epithelial to mesenchymal transition and the maintenance of CSCs-like properties. Overexpression of miR-491 targeted G-protein-coupled receptor kinase-interacting protein 1 (GIT-1), which blocked the activation of NF-κB by the inhibition of extracellular signal-regulated kinases (ERKs). Such process attenuated the CSCs-like properties in HCC cells. Our results point to a previously undefined mechanism by which miR-491 decreases CSCs-like properties and help to identify potential targets for the therapy of HCCs.

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“…Others are deleterious or lethal [loss of polarity (7), detachment (8), ER stress (9)]. All of these cues are reconfigured aberrantly and heterogeneously during the early stages of breast-mammary cancer (10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

Sporadic activation of an oxidative stress-dependent NRF2–p53 signaling network in breast epithelial spheroids and premalignancies

Pereira

Burns

Lee

et al. 2019

Preprint

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ABSTRACTBreast–mammary epithelial cells experience different local environments during tissue development and tumorigenesis. Microenvironmental heterogeneity gives rise to distinct cell-regulatory states whose identity and importance are just beginning to be appreciated. Cellular states diversify when clonal 3D spheroids are cultured in basement membrane, and prior transcriptomic analyses identified a state associated with stress tolerance and poor response to anticancer therapeutics. Here, we examined the regulation of this state and found that it is jointly coordinated by the NRF2 and p53 pathways, which are co-stabilized by spontaneous oxidative stress within the 3D cultures. Inhibition of NRF2 or p53 individually disrupts some of the transcripts defining the regulatory state but does not yield a notable phenotype in nontransformed breast epithelial cells. In contrast, combined perturbation prevents 3D growth in an oxidative stress-dependent manner. By integrating systems models of NRF2 and p53 signaling together as a single oxidative-stress network, we recapitulate these observations and make predictions about oxidative stress profiles during 3D growth. Similar coordination of NRF2 and p53 signaling is observed in normal breast epithelial tissue and hormone-negative ductal carcinoma in situ lesions. However, the pathways are uncoupled in triple-negative breast cancer, a subtype in which p53 is usually mutated. Using the integrated model, we reconcile the different NRF2-knockdown phenotypes of triple-negative cancer lines with their inferred handling of oxidative stress. Our results point to an oxidative stress-tolerance network that is important for single cells during glandular development and the early stages of breast cancer.One Sentence SummaryReactive oxygen species co-stabilize a non-oncogene and a tumor suppressor for triple-negative breast cancer when cells are surrounded by basement-membrane ECM.

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Stress signaling and the shaping of the mammary tissue in development and cancer

Cited by 32 publications

References 110 publications

Oxidative Stress and Carcinogenesis: Potential of Phytochemicals in Breast Cancer Therapy

Oxidative Stress and Carcinogenesis: Potential of Phytochemicals in Breast Cancer Therapy

MiR-491 attenuates cancer stem cells-like properties of hepatocellular carcinoma by inhibition of GIT-1/NF-κB-mediated EMT

Sporadic activation of an oxidative stress-dependent NRF2–p53 signaling network in breast epithelial spheroids and premalignancies

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