Molecular regulation of autophagy in a pro-inflammatory tumour microenvironment: New insight into the role of serum amyloid A

Plessis, Manisha du; Davis, Tanja Andrea; Loos, Ben; Pretorius, Etheresia; Villiers, Willem J.S. de; Engelbrecht, Anna‐Mart

doi:10.1016/j.cytogfr.2021.01.007

Cited by 11 publications

(11 citation statements)

References 131 publications

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“…MAPK includes ERK1/2, p38, and JNK. They can induce many cellular responses, such as proliferation, invasiveness, differentiation, and autophagy [ 153 , 154 ]. The role of abnormal activation of the RTK/Ras/MAPK/ERK pathway through genetic alterations in cancer has been extensively investigated [ 151 ].…”

Section: Tau In Glioblastomamentioning

confidence: 99%

Tau Protein as Therapeutic Target for Cancer? Focus on Glioblastoma

Hedna

Kovacic

Pagano

et al. 2022

Cancers

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Despite being extensively studied for several decades, the microtubule-associated protein Tau has not finished revealing its secrets. For long, Tau has been known for its ability to promote microtubule assembly. A less known feature of Tau is its capability to bind to cancer-related protein kinases, suggesting a possible role of Tau in modulating microtubule-independent cellular pathways that are associated with oncogenesis. With the intention of finding new therapeutic targets for cancer, it appears essential to examine the interaction of Tau with these kinases and their consequences. This review aims at collecting the literature data supporting the relationship between Tau and cancer with a particular focus on glioblastoma tumors in which the pathological significance of Tau remains largely unexplored. We will first treat this subject from a mechanistic point of view showing the pivotal role of Tau in oncogenic processes. Then, we will discuss the involvement of Tau in dysregulating critical pathways in glioblastoma. Finally, we will outline promising strategies to target Tau protein for the therapy of glioblastoma.

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Section: Tau In Glioblastomamentioning

confidence: 99%

Tau Protein as Therapeutic Target for Cancer? Focus on Glioblastoma

Hedna

Kovacic

Pagano

et al. 2022

Cancers

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“…Dysregulation of autophagy can initiate the transformation of normal cells to premalignant via metabolic stress, DNA damage, oxidative stress, and endoplasmic reticulum stress. In addition, autophagy can support the survival of transformed cells [ 23 ]. For instance, the type A receptor of IL-17 directly triggers pro-carcinogenic signaling in transformed enterocytes.…”

Section: The Role Of Chronic Inflammation In Different Stages Of Carcinogenesismentioning

confidence: 99%

Flavonoids against non-physiologic inflammation attributed to cancer initiation, development, and progression—3PM pathways

et al. 2021

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Inflammation is an essential pillar of the immune defense. On the other hand, chronic inflammation is considered a hallmark of cancer initiation and progression. Chronic inflammation demonstrates a potential to induce complex changes at molecular, cellular, and organ levels including but not restricted to the stagnation and impairment of healing processes, uncontrolled production of aggressive ROS/RNS, triggered DNA mutations and damage, compromised efficacy of the DNA repair machinery, significantly upregulated cytokine/chemokine release and associated patho-physiologic protein synthesis, activated signaling pathways involved in carcinogenesis and tumor progression, abnormal tissue remodeling, and created pre-metastatic niches, among others. The anti-inflammatory activities of flavonoids demonstrate clinically relevant potential as preventive and therapeutic agents to improve individual outcomes in diseases linked to the low-grade systemic and chronic inflammation, including cancers. To this end, flavonoids are potent modulators of pro-inflammatory gene expression being, therefore, of great interest as agents selectively suppressing molecular targets within pro-inflammatory pathways. This paper provides in-depth analysis of anti-inflammatory properties of flavonoids, highlights corresponding mechanisms and targeted molecular pathways, and proposes potential treatment models for multi-level cancer prevention in the framework of predictive, preventive, and personalized medicine (PPPM / 3PM). To this end, individualized profiling and patient stratification are essential for implementing targeted anti-inflammatory approaches. Most prominent examples are presented for the proposed application of flavonoid-conducted anti-inflammatory treatments in overall cancer management.

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“…For preexposure prophylaxis, the monoclonal antibody combinations of tixagevimab plus cilgavimab also have an EUA from the FDA for populations who are immunocompromised and with limited expected response to vaccination [13]. This is important because unvaccinated and immunocompromised patients are at most risk for severe COVID-19 including ARDS [14][15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

Rationale of using the dual chemokine receptor CCR2/CCR5 inhibitor cenicriviroc for the treatment of COVID-19

et al. 2022

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Coronavirus Disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), has created a global pandemic infecting over 230 million people and costing millions of lives. Therapies to attenuate severe disease are desperately needed. Cenicriviroc (CVC), a C-C chemokine receptor type 5 (CCR5) and C-C chemokine receptor type 2 (CCR2) antagonist, an agent previously studied in advanced clinical trials for patients with HIV or nonalcoholic steatohepatitis (NASH), may have the potential to reduce respiratory and cardiovascular organ failures related to COVID-19. Inhibiting the CCR2 and CCR5 pathways could attenuate or prevent inflammation or fibrosis in both early and late stages of the disease and improve outcomes of COVID-19. Clinical trials using CVC either in addition to standard of care (SoC; e.g., dexamethasone) or in combination with other investigational agents in patients with COVID-19 are currently ongoing. These trials intend to leverage the anti-inflammatory actions of CVC for ameliorating the clinical course of COVID-19 and prevent complications. This article reviews the literature surrounding the CCR2 and CCR5 pathways, their proposed role in COVID-19, and the potential role of CVC to improve outcomes.

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Molecular regulation of autophagy in a pro-inflammatory tumour microenvironment: New insight into the role of serum amyloid A

Cited by 11 publications

References 131 publications

Tau Protein as Therapeutic Target for Cancer? Focus on Glioblastoma

Tau Protein as Therapeutic Target for Cancer? Focus on Glioblastoma

Flavonoids against non-physiologic inflammation attributed to cancer initiation, development, and progression—3PM pathways

Rationale of using the dual chemokine receptor CCR2/CCR5 inhibitor cenicriviroc for the treatment of COVID-19

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