Duality of bone morphogenetic proteins in cancer: A comprehensive analysis

Sharma, Tanu; Kapoor, Anmol; Mandal, Chandi C.

doi:10.1002/jcp.30785

Cited by 10 publications

(9 citation statements)

References 254 publications

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“…BMP signaling is involved in a wide range of cellular process, and its role in tumor growth and metastasis are controversial. Plentiful of studies have reported that BMPs may either play pro-tumorigenic roles via enhancing cell proliferation, motility, and invasion in cancers or, on the contrary, suppress the metastasis of cancer cells 39 . These reports suggest that BMPs function in a context dependent manner, and switch the oncogenic or tumor-suppressive role under certain conditions, however, the underlying mechanism remains unrevealed.…”

Section: Discussionmentioning

confidence: 99%

GALNT12 suppresses the bone-specific prostate cancer metastasis by activating BMP pathway via the O-glycosylation of BMPR1A

Yang,

Ding,

Yin

et al. 2024

Int. J. Biol. Sci.

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Bone metastasis caused the majority death of prostate cancer (PCa) but the mechanism remains poorly understood. In this present study, we show that polypeptide N-acetylgalactosaminyltransferase 12 (GALNT12) suppresses bone-specific metastasis of PCa. GALNT12 suppresses proliferation, migration, invasion and cell division ability of PCa cells by activating the BMP pathway. Mechanistic investigations showed that GALNT12 augments the O-glycosylation of BMPR1A then actives the BMP pathway. Activated BMP signaling inhibits the expression of integrin αVβ3 to reduce the bone-specific seeding of PCa cells. Furthermore, activated BMP signaling remolds the immune microenvironment by suppressing the STAT3 pathway. Our results of this study illustrate the role and mechanism of GALNT12 in the process of bone metastasis of PCa and identify GALNT12 as a potential therapeutic target for metastatic PCa.

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Section: Discussionmentioning

confidence: 99%

GALNT12 suppresses the bone-specific prostate cancer metastasis by activating BMP pathway via the O-glycosylation of BMPR1A

Yang,

Ding,

Yin

et al. 2024

Int. J. Biol. Sci.

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“…As a result of Wnt -pathway upregulation, the interconnected loop of BMP signaling becomes dysregulated [ 234 , 235 ]. BMPs have been found to act as TSs in Renal Cell Carcinoma, Glioblastoma, esophageal adenocarcinoma, prostate adenocarcinoma, diffuse gastric adenocarcinoma and others [ 236 , 237 ].…”

Section: Key Cardiac Signaling Pathwaysmentioning

confidence: 99%

The benign nature and rare occurrence of cardiac myxoma as a possible consequence of the limited cardiac proliferative/ regenerative potential: a systematic review

Shafi,

Siddiqui,

Jaffry

2023

BMC Cancer

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Background Cardiac Myxoma is a primary tumor of heart. Its origins, rarity of the occurrence of primary cardiac tumors and how it may be related to limited cardiac regenerative potential, are not yet entirely known. This study investigates the key cardiac genes/ transcription factors (TFs) and signaling pathways to understand these important questions. Methods Databases including PubMed, MEDLINE, and Google Scholar were searched for published articles without any date restrictions, involving cardiac myxoma, cardiac genes/TFs/signaling pathways and their roles in cardiogenesis, proliferation, differentiation, key interactions and tumorigenesis, with focus on cardiomyocytes. Results The cardiac genetic landscape is governed by a very tight control between proliferation and differentiation-related genes/TFs/pathways. Cardiac myxoma originates possibly as a consequence of dysregulations in the gene expression of differentiation regulators including Tbx5, GATA4, HAND1/2, MYOCD, HOPX, BMPs. Such dysregulations switch the expression of cardiomyocytes into progenitor-like state in cardiac myxoma development by dysregulating Isl1, Baf60 complex, Wnt, FGF, Notch, Mef2c and others. The Nkx2–5 and MSX2 contribute predominantly to both proliferation and differentiation of Cardiac Progenitor Cells (CPCs), may possibly serve roles based on the microenvironment and the direction of cell circuitry in cardiac tumorigenesis. The Nkx2–5 in cardiac myxoma may serve to limit progression of tumorigenesis as it has massive control over the proliferation of CPCs. The cardiac cell type-specific genetic programming plays governing role in controlling the tumorigenesis and regenerative potential. Conclusion The cardiomyocytes have very limited proliferative and regenerative potential. They survive for long periods of time and tightly maintain the gene expression of differentiation genes such as Tbx5, GATA4 that interact with tumor suppressors (TS) and exert TS like effect. The total effect such gene expression exerts is responsible for the rare occurrence and benign nature of primary cardiac tumors. This prevents the progression of tumorigenesis. But this also limits the regenerative and proliferative potential of cardiomyocytes. Cardiac Myxoma develops as a consequence of dysregulations in these key genes which revert the cells towards progenitor-like state, hallmark of CM. The CM development in carney complex also signifies the role of TS in cardiac cells.

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“…As a result of Wnt-pathway upregulation, the interconnected loop of BMP signaling becomes dysregulated [236,237]. BMPs have been found to act as tumor suppressors in RCC, GBM, esophageal adenocarcinoma, prostate adenocarcinoma, diffuse gastric adenocarcinoma and others [238,239]. The role of BMPs in hepatocellular carcinoma is different and of immense signi cance as these cells have vast regenerative potential.…”

Section: Role In Proliferation Differentiation and In Tumorigenesismentioning

confidence: 99%

The benign nature and rare occurrence of cardiac myxoma as a possible consequence of the limited cardiac proliferative/ regenerative potential: a systematic review

Shafi

Siddiqui

Jaffry

2022

Preprint

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Background: Cardiac Myxoma (CM) is a primary tumor of heart. Its origins, why the occurrence of primary cardiac tumors is extremely rare and how it may be related to limited cardiac regenerative potential, these aspects are not yet entirely known. This study investigates the key cardiac genes/TFs and signaling pathways to advance our understanding of these important questions. Methods: Databases including PubMed, MEDLINE, and Google Scholar were searched for published articles without any date restrictions, involving cardiac myxoma, cardiac genes/TFs/signaling pathways and their roles in cardiogenesis, proliferation, differentiation, key interactions and tumorigenesis, with focus on cardiomyocytes. Results: The cardiac genetic landscape is governed by a very tight control between proliferation and differentiation-related genes/TFs/pathways. Cardiac myxoma originates possibly as a consequence of dysregulations in the gene expression of differentiation regulators including Tbx5, GATA4, HAND1/2, MYOCD, HOPX, BMPs. Such dysregulations switch the expression of cardiomyocytes into progenitor-like state in cardiac myxoma development by dysregulating Isl1, Baf60 complex, Wnt, FGF, Notch, Mef2c and others. The Nkx2-5 and MSX2 contribute to both proliferation and differentiation of Cardiac Progenitor Cells (CPCs) may possibly serve roles based on the microenvironment and the direction of cell circuitry in cardiac tumorigenesis. The Nkx2-5 in cardiac myxoma may serve to limit progression of tumorigenesis as it has massive control over the proliferation of CPCs. The cardiac cell type-specific genetic programming plays governing role in controlling the tumorigenesis and regenerative potential. Conclusion: The cardiomyocytes have very limited proliferative and regenerative potential. They survive for long periods of time and tightly maintain the gene expression of differentiation genes such as Tbx5, GATA4 that interact with tumor suppressors (TS) and exert TS like effect. The total effect such gene expression exerts is responsible for the rare occurrence and benign nature of primary cardiac tumors. This prevents the progression of tumorigenesis. But this also limits the regenerative and proliferative potential of cardiomyocytes. Cardiac Myxoma (CM) develops as a consequence of dysregulations in these key genes which revert the cells towards progenitor-like state, hallmark of CM. The CM development in carney complex also signifies the role of TS in cardiac cells.

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Duality of bone morphogenetic proteins in cancer: A comprehensive analysis

Cited by 10 publications

References 254 publications

GALNT12 suppresses the bone-specific prostate cancer metastasis by activating BMP pathway via the O-glycosylation of BMPR1A

GALNT12 suppresses the bone-specific prostate cancer metastasis by activating BMP pathway via the O-glycosylation of BMPR1A

The benign nature and rare occurrence of cardiac myxoma as a possible consequence of the limited cardiac proliferative/ regenerative potential: a systematic review

The benign nature and rare occurrence of cardiac myxoma as a possible consequence of the limited cardiac proliferative/ regenerative potential: a systematic review

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