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1.
Clin. transl. oncol. (Print) ; 25(10): 2763-2771, oct. 2023.
Article in English | IBECS | ID: ibc-225057

ABSTRACT

The continuous increase in cancer-associated deaths despite the substantial improvement in diagnosis and treatment has sparked discussions on the need for novel biomarkers and therapeutic strategies for cancer. Although increasing evidence has demonstrated the pivotal role of relaxin-2 in multiple cancers, their role is a double-edged sword with both protumor and antitumor having been reported in various malignant tumors. Considering this dual role, it appears the biological mechanism underpinning the action of relaxin-2 in cancer is not clear and further studies to elucidate their potential as a preventive factor for cancers are of prime importance. Herein, a summarized up-to-date report on the role of relaxin-2 in human cancer including detailed clinical and experimental evidence supporting their tumor-promoting and inhibitory functions in cancer development and progression has been elucidated. Also, signaling pathways and other factors orchestrating the activities of relaxin-2 in the tumor microenvironment has been discussed. Collectively, the evidence from this review has demonstrated the need for further evaluation of the role of relaxin-2 as a diagnostic and or prognostic biomarker for cancer (AU)


Subject(s)
Humans , Neoplasms , Relaxin/metabolism , Relaxin/pharmacology , Signal Transduction , Tumor Microenvironment
2.
Clin. transl. oncol. (Print) ; 25(7): 1963-1976, jul. 2023. ilus
Article in English | IBECS | ID: ibc-222371

ABSTRACT

Neutrophils have emerged as important players in the tumor microenvironment, largely attributed to their plasticity and heterogeneity. Evidence accumulated thus far indicates that neutrophils signaled by external cues can promote tumor progression via several mechanisms. Hence, in our quest to target tumor-associated neutrophils to improve treatment, understanding the mechanisms by which tumor-derived factors regulate neutrophils to gain pro-tumor functions and the feedback loop by which these neutrophils promote tumor progression is very crucial. Herein, we review the published data on how tumor-derived factors alter neutrophils phenotype to promote tumor progression with particular emphasis on immunosuppression, autophagy, angiogenesis, tumor proliferation, metastasis, and therapeutic resistance. These deeper insights could provide a wider view and novel therapeutic approach to neutrophil-targeted therapy in cancer (AU)


Subject(s)
Humans , Neoplasms/pathology , Neoplasms/therapy , Neutrophils/pathology , Tumor Microenvironment , Immunosuppression Therapy , Autophagy
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