Repurposing of drugs as STAT3 inhibitors for cancer therapy

Thilakasiri, Pathum; Dmello, Rhynelle S.; Nero, Tracy L.; Parker, Michael W.; Ernst, Matthias; Chand, Ashwini L.

doi:10.1016/j.semcancer.2019.09.022

Cited by 68 publications

(47 citation statements)

References 169 publications

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“…There are actually some challenges regarding the STAT-3-based therapies in the clinic. Firstly, there are large sequence and conformational similarities between STAT-3 and other STAT members such as STAT-1 and STAT-5 [ 111 ]. Biologically, STAT-1 and STAT-3 exert opposite activities.…”

Section: Discussionmentioning

confidence: 99%

Contribution of STAT3 to the pathogenesis of COVID-19

Jafarzadeh

Nemati

Jafarzadeh

2021

Microbial Pathogenesis

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Hyper-inflammatory responses, lymphopenia, unbalanced immune responses, cytokine storm, large viral replication and massive cell death play fundamental roles in the pathogenesis of COVID-19. Extreme production of many kinds of pro-inflammatory cytokines and chemokines occur in severe COVID-19 that called cytokine storm. Signal transducer and activator of transcription-3 (STAT-3) present in the cytoplasm in an inactive form and can be stimulated by a vast range of cytokines, chemokines and growth factors. Thus, STAT-3 can participate in the induction of inflammatory responses during coronavirus infections. STAT-3 can also suppress anti-virus interferon response and induce unbalanced anti-virus adaptive immune response, through influencing Th17-, Th1-, Treg-, and B cell-mediated functions. Furthermore, STAT-3 can contribute to the M2 macrophage polarization, lung fibrosis and thrombosis. Moreover, STAT-3 may be directly targeted by some virus-derived protein and operate as a pro-viral or anti-viral element in a virus-specific process. Here, the possible contribution of STAT-3 to the pathogenesis of COVID-19 was explained, while providing potential approaches to target this transcription factor in an attempt for COVID-19 treatment.

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Section: Discussionmentioning

confidence: 99%

Contribution of STAT3 to the pathogenesis of COVID-19

Jafarzadeh

Nemati

Jafarzadeh

2021

Microbial Pathogenesis

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“…The in vitro and in vivo experiments manifest that RHOC enhanced the proliferative and invasive capacity of esophageal cancer cells[ 25 ]. Similar to RHOC, STAT3 is a pivotal molecule that accelerates development and progression of malignant tumors[ 26 , 27 ]. In esophageal cancer cells, activation of STAT3 dramatically reduced apoptotic rate and contributed to increased proliferative ability[ 28 ].…”

Section: Discussionmentioning

confidence: 99%

Circular RNA AKT3 governs malignant behaviors of esophageal cancer cells by sponging miR-17-5p

Zang¹,

Ji²,

Ju³

et al. 2021

WJG

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“…Activating STAT3 is essential for C1orf61-induced cellular EMT and migration Signal transducer and activator of transcription 3 (STAT3) is a transcription factor involved in a major cascade responsive to stimulation by many growth factors and cytokines. [21] STAT3 is involved in the regulation of cell proliferation, apoptosis, cell invasion, angiogenesis and EMT processes. [22][23][24] Hence, we determined the levels of STAT3 and phosphorylated-STAT3.…”

Section: C1orf61 Regulates Emt-related Gene Expression and Induces Cementioning

confidence: 99%

C1orf61 promotes hepatocellular carcinoma metastasis and affects the therapeutic response to sorafenib

Wang

Huang

et al. 2020

Preprint

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Background C1orf61 is a specific transcriptional activator that is highly up-regulated during weeks 4–9 of human embryogenesis, the period in which most organs develop. We have previously demonstrated that C1orf61 acts as a tumor activator in human hepatocellular carcinoma (HCC) tumorigenesis and metastasis. However, the underlying molecular mechanisms of tumor initiation and progression in HCC remain obscure. Methods In this study, we demonstrated that the pattern of C1orf61 expression was closely correlated with metastasis in liver cancer cells. Gene expression profiling analysis indicated that C1orf61 regulated diverse genes related to cell growth, migration, invasion and epithelial-mesenchymal transition (EMT). Results Results showed that C1orf61 promotes hepatocellular carcinoma metastasis by inducing cellular EMT in vivo and in vitro. Moreover, C1orf61-induced cellular EMT and migration are involved in the activation of the STAT3 and Akt cascade pathways. We also found that C1orf61 was associated with HBV infection-induced cell migration in HCC. In addition, C1orf61 expression improved the efficacy of the anticancer therapy sorafenib in HCC patients. For the first time, we report a regulatory pathway by which C1orf61 promoted cancer cell metastasis and regulated the therapeutic response to sorafenib. Conclusions These findings increased our understanding of the molecular events that regulate metastasis and treatment in HCC.

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Repurposing of drugs as STAT3 inhibitors for cancer therapy

Cited by 68 publications

References 169 publications

Contribution of STAT3 to the pathogenesis of COVID-19

Contribution of STAT3 to the pathogenesis of COVID-19

Circular RNA AKT3 governs malignant behaviors of esophageal cancer cells by sponging miR-17-5p

C1orf61 promotes hepatocellular carcinoma metastasis and affects the therapeutic response to sorafenib

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