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Hydrogen sulfide and carbon monoxide as possible regulators of YY1 and RKIP: Novel insights into gastrointestinal
Edyta Korbut1, Małgorzata Lasota2, Daniel Jankowski2
1Center for Biomedicine and Interdisciplinary Sciences, Jagiellonian University Medical College, Krakow, Poland.
Abstract:
Gastrointestinal (GI) cancers remain among the leading causes of cancer-related mortality, with challenges in early detection, therapeutic resistance, and poor prognosis. Two key molecular players, Yin Yang 1 (YY1) and Raf kinase inhibitor protein (RKIP), have emerged as important regulators of cancer progression and treatment response. This review highlights their individual and interactive roles across various GI malignancies, including gastric, colorectal, pancreatic, and liver cancers. Evidence indicates an antagonistic relationship, where YY1 promotes tumor growth and epithelial-mesenchymal transition (EMT), while RKIP counters these effects by suppressing oncogenic signaling pathways. On the other hand, endogenous gaseous transmitter, nitric oxide (NO) has been clearly shown to influence the YY1-RKIP axis. NO directly inhibits YY1 via S-nitrosylation and promotes RKIP expression, reinforcing pro-apoptotic and anti-metastatic pathways. Although some scientific evidence exists, the role of another gaseous mediator, hydrogen sulfide (H₂S), as a modulator of YY1 or RKIP remains poorly characterized. Its regulatory influence, especially via interaction with NO signaling, suggests a complex, context-dependent role. H2S/sulfides-mediated posttranslational modification of proteins - persulfidation - has been shown recently to be functionally important but not in the context of YY1 or RKIP activity. Moreover, carbon monoxide (CO) that interacts with metalloproteins has been completely overlooked as possible regulator of YY1/RKIP-dependent cancer biology. Therefore, we indicate here the possible interplay between H2S and CO with YY1/RKIP that may provide new further scientific direction in this field, based on aggressive GI tumors.
Insights
Yin Yang 1 (YY1) and Raf kinase inhibitor protein (RKIP) regulate gastrointestinal cancers. Nitric oxide (NO) impacts this axis, while hydrogen sulfide (H₂S) and carbon monoxide (CO) roles require further study.
Area of Science:
- Oncology
- Molecular Biology
- Gastroenterology
Background:
- Gastrointestinal (GI) cancers are a leading cause of mortality, often presenting challenges in early detection and treatment resistance.
- Yin Yang 1 (YY1) and Raf kinase inhibitor protein (RKIP) are key regulators of cancer progression and treatment response in GI malignancies.
- An antagonistic relationship exists between YY1 (oncogenic) and RKIP (tumor suppressive), influencing tumor growth and epithelial-mesenchymal transition (EMT).
Purpose of the Study:
- To review the individual and interactive roles of YY1 and RKIP in GI cancers.
- To explore the influence of endogenous gaseous transmitters, including nitric oxide (NO), hydrogen sulfide (H₂S), and carbon monoxide (CO), on the YY1-RKIP axis.
- To identify potential new research directions for targeting the YY1-RKIP pathway in aggressive GI tumors.
Main Methods:
- Literature review of existing scientific evidence on YY1, RKIP, and gaseous transmitters in GI cancer.
- Analysis of the molecular mechanisms by which NO affects YY1 and RKIP.
- Identification of knowledge gaps regarding the roles of H₂S and CO in modulating the YY1-RKIP axis.
Main Results:
- YY1 promotes tumor growth and EMT, while RKIP suppresses these processes.
- Nitric oxide (NO) directly inhibits YY1 via S-nitrosylation and upregulates RKIP expression, enhancing anti-cancer pathways.
- The roles of hydrogen sulfide (H₂S) and carbon monoxide (CO) in regulating YY1 and RKIP in GI cancers are largely uncharacterized but hold potential significance.
Conclusions:
- The YY1-RKIP axis is a critical regulator in GI cancers, modulated by NO.
- Further investigation into the roles of H₂S and CO in the YY1-RKIP pathway could reveal novel therapeutic strategies for aggressive GI tumors.
- Understanding these complex interactions may lead to improved early detection and treatment of GI malignancies.
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