TY - JOUR
T1 - Harnessing the tumor microenvironment
T2 - targeted cancer therapies through modulation of epithelial-mesenchymal transition
AU - Glaviano, Antonino
AU - Lau, Hannah Si-Hui
AU - Carter, Lukas M.
AU - Lee, E. Hui Clarissa
AU - Lam, Hiu Yan
AU - Okina, Elena
AU - Tan, Donavan Jia Jie
AU - Tan, Wency
AU - Ang, Hui Li
AU - Carbone, Daniela
AU - Yee, Michelle Yi-Hui
AU - Shanmugam, Muthu K.
AU - Huang, Xiao Zi
AU - Sethi, Gautam
AU - Tan, Tuan Zea
AU - Lim, Lina H. K.
AU - Huang, Ruby Yun-Ju
AU - Ungefroren, Hendrik
AU - Giovannetti, Elisa
AU - Tang, Dean G.
AU - Bruno, Tullia C.
AU - Luo, Peng
AU - Andersen, Mads Hald
AU - Qian, Bin-Zhi
AU - Ishihara, Jun
AU - Radisky, Derek C.
AU - Elias, Salem
AU - Yadav, Saurabh
AU - Kim, Minah
AU - Robert, Caroline
AU - Diana, Patrizia
AU - Schalper, Kurt A.
AU - Shi, Tao
AU - Merghoub, Taha
AU - Krebs, Simone
AU - Kusumbe, Anjali P.
AU - Davids, Matthew S.
AU - Brown, Jennifer R.
AU - Kumar, Alan Prem
N1 - Publisher Copyright:
© The Author(s) 2025.
PY - 2025/12
Y1 - 2025/12
N2 - The tumor microenvironment (TME) is integral to cancer progression, impacting metastasis and treatment response. It consists of diverse cell types, extracellular matrix components, and signaling molecules that interact to promote tumor growth and therapeutic resistance. Elucidating the intricate interactions between cancer cells and the TME is crucial in understanding cancer progression and therapeutic challenges. A critical process induced by TME signaling is the epithelial-mesenchymal transition (EMT), wherein epithelial cells acquire mesenchymal traits, which enhance their motility and invasiveness and promote metastasis and cancer progression. By targeting various components of the TME, novel investigational strategies aim to disrupt the TME's contribution to the EMT, thereby improving treatment efficacy, addressing therapeutic resistance, and offering a nuanced approach to cancer therapy. This review scrutinizes the key players in the TME and the TME's contribution to the EMT, emphasizing avenues to therapeutically disrupt the interactions between the various TME components. Moreover, the article discusses the TME's implications for resistance mechanisms and highlights the current therapeutic strategies toward TME modulation along with potential caveats.
AB - The tumor microenvironment (TME) is integral to cancer progression, impacting metastasis and treatment response. It consists of diverse cell types, extracellular matrix components, and signaling molecules that interact to promote tumor growth and therapeutic resistance. Elucidating the intricate interactions between cancer cells and the TME is crucial in understanding cancer progression and therapeutic challenges. A critical process induced by TME signaling is the epithelial-mesenchymal transition (EMT), wherein epithelial cells acquire mesenchymal traits, which enhance their motility and invasiveness and promote metastasis and cancer progression. By targeting various components of the TME, novel investigational strategies aim to disrupt the TME's contribution to the EMT, thereby improving treatment efficacy, addressing therapeutic resistance, and offering a nuanced approach to cancer therapy. This review scrutinizes the key players in the TME and the TME's contribution to the EMT, emphasizing avenues to therapeutically disrupt the interactions between the various TME components. Moreover, the article discusses the TME's implications for resistance mechanisms and highlights the current therapeutic strategies toward TME modulation along with potential caveats.
KW - Cancer
KW - Cancer-associated fibroblasts (CAFs)
KW - Chimeric antigen-receptor (CAR) T-cell therapy
KW - Dendritic cells (DCs)
KW - Epithelial-mesenchymal transition (EMT)
KW - Extracellular matrix (ECM)
KW - Metastasis
KW - Myeloid-derived suppressor cells (MDSCs)
KW - Natural killer (NK) cells
KW - T-cell receptor (TCR) therapy
KW - T-cells, B-cells, tumor-associated macrophages (TAMs)
KW - Theranostics
KW - Tumor microenvironment (TME)
KW - Tumor-associated neutrophils (TANs)
UR - https://www.scopus.com/pages/publications/85215538883
U2 - 10.1186/s13045-024-01634-6
DO - 10.1186/s13045-024-01634-6
M3 - Review article
C2 - 39806516
SN - 1756-8722
VL - 18
SP - 6
JO - Journal of hematology & oncology
JF - Journal of hematology & oncology
IS - 1
M1 - 6
ER -
