Inflammation-induced oxidative stress in breast cancer patients

Roque, Aline Tengan; Gambeloni, Rafael Zuppardo; Felitti, Simone; Ribeiro, Marcelo Lima; Santos, Juliana C.

doi:10.1007/s12032-015-0709-5

Cited by 26 publications

(14 citation statements)

References 19 publications

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“…24 Continued oxidative stress can lead to inflammation, which can further mediate most chronic diseases including cancer, diabetes, cardiovascular and pulmonary diseases. 25 The nuclear factor erythroid 2-related factor 2 (Nrf2) pathway plays an imperative role in cellular redox homeostasis, and the activation of this pathway is one of the main defense mechanisms against oxidative stress. In the present study, we found that betulin has anti-inflammatory potential via its activation of the Nrf2 pathway, and this activation of Nrf2 is AMPK-dependent in a LPS-challenged inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

Betulin exhibits anti-inflammatory activity in LPS-stimulated macrophages and endotoxin-shocked mice through an AMPK/AKT/Nrf2-dependent mechanism

Zhou

et al. 2017

Cell Death Dis

103

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Continued oxidative stress can lead to chronic inflammation, which in turn could mediate most chronic diseases including cancer. Nuclear factor erythroid 2-related factor (Nrf2), a critical transcriptional activator for antioxidative responses, has envolved to be an attractive drug target for the treatment or prevention of human diseases. In the present study, we investigated the effects and mechanisms of betulin on Nrf2 activation and its involvement in the lipopolysaccharide (LPS)-triggered inflammatory system. In macrophages, betulin activated the Nrf2 signaling pathway and increased Nrf2-targeted antioxidant and detoxifying enzymes, including NADPH, quinine oxidoreductase 1 (NQO1), heme oxygenase-1 (HO-1), γ-glutamyl cysteine synthetase catalytic subunit (GCLC) and modifier subunit (GCLM) in a dose and time dependent manner. Importantly, we found betulin-induced activation of Nrf2 is AMPK/AKT/GSK3β dependent, as pharmacologically inactivating AMPK blocked the activating effect of betulin on AKT, GSK3β and Nrf2. Furthermore, betulin attenuated LPS-induced inflammatory mediators (iNOS and COX-2) and MAPK inflammatory signaling pathway. The effect of betulin on HO-1 and NQO1 upregulation, iNOS and COX-2 the downregulation, and survival time extension was largely weakened when Nrf2 was depleted in vitro and in vivo. Our results demonstrate that the AMPK/AKT/Nrf2 pathways are essential for the anti-inflammatory effects of betulin in LPS-stimulated macrophages and endotoxin-shocked mice.

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Section: Discussionmentioning

confidence: 99%

Betulin exhibits anti-inflammatory activity in LPS-stimulated macrophages and endotoxin-shocked mice through an AMPK/AKT/Nrf2-dependent mechanism

Zhou

et al. 2017

Cell Death Dis

103

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“…64 Recent study conducted in breast cancer tissues shows increased expression of inflammatory cytokines like COX-2, IL-1β, IL-8, and TNF-α compared to the normal tissues. 65 Moreover, the study showed increased expression of ROS and DNA damage in cancer tissues. Another study showed increased breast cancer incidence in patients who have taken oral contraceptives.…”

Section: Ros Induced Change In Inflammationmentioning

confidence: 94%

Role of oxidative stress in facilitating carcinogenesis

Natarajan

2017

Int J Res Med Sci

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The carcinogenic role of ROS has been a great debate in the past and will be in the future. ROS is produced by both internal (inflammation) and external sources (UV). ROS is important for various important signalling mechanisms for the normal cellular survival. Even though literature exists to support the role of ROS in cancer, the magnitude of its expression and cell type it is expressed will determine whether it plays a positive (apoptosis) or negative role (genomic instability) in cancer. Apart from inducing DNA damage, ROS facilitates carcinogenesis by regulating cell cycle progression, gap junction, inflammation etc. The present review updates the recent discoveries of how ROS regulates these important cellular signalling mechanisms to facilitate carcinogenesis.

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“…First, the intrinsic and extrinsic biological activities associated with tumours have likely been underestimated. Tumours may actively produce inflammatory mediators as a consequence of local oxidative stress or stimulate inflammation in response to their presence . These findings might account for baseline cognitive dysfunction.…”

Section: Neuroinflammation and Cognitive Dysfunctionmentioning

confidence: 99%

“…Tumours may actively produce inflammatory mediators as a consequence of local oxidative stress or stimulate inflammation in response to their presence. 116 These findings might account for baseline cognitive dysfunction. Nonetheless, the lack of significant differences in cytokine levels between recently diagnosed cancer patients and noncancer controls clouds definitive conclusions.…”

Section: Tumour-dependent Cytokine Productionmentioning

confidence: 99%

Cytokine‐mediated blood brain barrier disruption as a conduit for cancer/chemotherapy‐associated neurotoxicity and cognitive dysfunction

Wardill

Mander

Sebille

et al. 2016

Intl Journal of Cancer

132

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Publishing in a subscription based journal Accepted (peer-reviewed) VersionThe accepted version of an article is the version that incorporates all amendments made during the peer review process, but prior to the final published version (the Version of Record, which includes; copy and stylistic edits, online and print formatting, citation and other linking, deposit in abstracting and indexing services, and the addition of bibliographic and other material.Self-archiving of the accepted version is subject to an embargo period of 12-24 months. The embargo period is 12 months for scientific, technical, and medical (STM) journals and 24 months for social science and humanities (SSH) journals following publication of the final article.• the author's personal website • the author's company/institutional repository or archive • not for profit subject-based repositories such as PubMed Central Articles may be deposited into repositories on acceptance, but access to the article is subject to the embargo period. The version posted may not be updated or replaced with the final published version (the Version of Record). Authors may transmit, print and share copies of the accepted version with colleagues, provided that there is no systematic distribution, e.g. a posting on a listserve, network or automated delivery.There is no obligation upon authors to remove preprints posted to not for profit preprint servers prior to submission. and subsequent cognitive impairment. Emerging data now show detectable levels of some chemotherapeutic agents within the CNS, indicating potential disruption of blood brain barrier integrity or transport mechanisms. Blood brain barrier disruption is a key aspect of many neurocognitive disorders, particularly those characterised by a proinflammatory state. Importantly, many proinflammatory mediators able to modulate the blood brain barrier are generated by tissues and organs that are targets for chemotherapy-associated toxicities. This review therefore aims to explore the hypothesis that peripherally-derived inflammatory cytokines disrupt blood brain barrier permeability, thereby increasing direct access of chemotherapeutic agents into the CNS to facilitate neuroinflammation and central neurotoxicity. 60

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Inflammation-induced oxidative stress in breast cancer patients

Cited by 26 publications

References 19 publications

Betulin exhibits anti-inflammatory activity in LPS-stimulated macrophages and endotoxin-shocked mice through an AMPK/AKT/Nrf2-dependent mechanism

Betulin exhibits anti-inflammatory activity in LPS-stimulated macrophages and endotoxin-shocked mice through an AMPK/AKT/Nrf2-dependent mechanism

Role of oxidative stress in facilitating carcinogenesis

Cytokine‐mediated blood brain barrier disruption as a conduit for cancer/chemotherapy‐associated neurotoxicity and cognitive dysfunction

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