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(1) Wnt and BMP signaling in stem cell proliferation and differentiation. Wnt and BMP signaling pathways play an important role in development. Using pluripotent mesenchymal stem cells (MSCs) we have demonstrated that the 14 types of BMPs exhibit distinct roles in regulating linage commitments of MSCs. We have also illustrated the distinct functions of the 19 Wnt factors in regulating lineage-specific differentiation of MSCs. Furthermore, there is a cross-talk between Wnt and BMP pathways. We are interested in identifying the key signaling mediators that regulate stem cell differentiation and that control lineage divergences.
(2) Defects in stem cell differentiation and tumorigenesis. The essence of genetic and epigenetic changes in cancer cells is intended to disrupt the differentiation pathways. We have found that bone tumor cells fail to undergo terminal differentiation. In fact, the bone tumor cells are refractory to differentiation signals, and even convert differentiation cues into proliferation signals. We are interested in identifying critical differentiation defects that may hold keys to unlock tumorigenesis.
(3) Interactions between tumors and stromal cells in bone metastasis. Interactions between disseminated cancer cells and bone marrow stromal cells (aka bone marrow mesenchymal stem cells, bMSCs) may play an important role in controlling the survival and colonization of bone metastasis. Using bone metastasis animal models, we are interested in elucidating the roles of bMSC-derived factors in the development of bone metastasis.
(4) Targeted therapies and regenerative medicine. Identification of differentiation defects in tumors would allow us to develop novel differentiation therapies that circumvent the defective stages. Accordingly, the bMSC-derived factors may serve as cancer drug targets. The critical regulators of stem cell differentiation may be used for stem cell-based and/or gene therapies in tissue regeneration.
(1) Wnt and BMP signaling in stem cell proliferation and differentiation. Wnt and BMP signaling pathways play an important role in development. Using pluripotent mesenchymal stem cells (MSCs) we have demonstrated that the 14 types of BMPs exhibit distinct roles in regulating linage commitments of MSCs. We have also illustrated the distinct functions of the 19 Wnt factors in regulating lineage-specific differentiation of MSCs. Furthermore, there is a cross-talk between Wnt and BMP pathways. We are interested in identifying the key signaling mediators that regulate stem cell differentiation and that control lineage divergences.
(2) Defects in stem cell differentiation and tumorigenesis. The essence of genetic and epigenetic changes in cancer cells is intended to disrupt the differentiation pathways. We have found that bone tumor cells fail to undergo terminal differentiation. In fact, the bone tumor cells are refractory to differentiation signals, and even convert differentiation cues into proliferation signals. We are interested in identifying critical differentiation defects that may hold keys to unlock tumorigenesis.
(3) Interactions between tumors and stromal cells in bone metastasis. Interactions between disseminated cancer cells and bone marrow stromal cells (aka bone marrow mesenchymal stem cells, bMSCs) may play an important role in controlling the survival and colonization of bone metastasis. Using bone metastasis animal models, we are interested in elucidating the roles of bMSC-derived factors in the development of bone metastasis.
(4) Targeted therapies and regenerative medicine. Identification of differentiation defects in tumors would allow us to develop novel differentiation therapies that circumvent the defective stages. Accordingly, the bMSC-derived factors may serve as cancer drug targets. The critical regulators of stem cell differentiation may be used for stem cell-based and/or gene therapies in tissue regeneration.
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AMERICAN JOURNAL OF CANCER RESEARCHno. 3 (2023): 1137-1139
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Genes and Diseasesno. 2 (2023): 627-629
Mary Rose Rogers,Wei Zeng, Xian Zhang,Ruidong Li,Qiang Wei,Yuhan Kong,Piao Zhao,Guozhi Zhao,Yonghui Wang,Jiamin Zhong, Yi Zhu,Rex C. Haydon,
Genes & Diseasesno. 4 (2023): 1175-1179
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