Results 181 to 190 of about 254,320 (258)
Chronic TGF‐β exposure drives epithelial HCC cells from a senescent state to a TGF‐β resistant mesenchymal phenotype. This transition is characterized by the loss of Smad3‐mediated signaling, escape from senescence, enhanced invasiveness and metastatic potential, and upregulation of key resistance modulators such as MARK1 and GRM8, ultimately promoting
Minenur Kalyoncu+11 more
wiley +1 more source
We identified adaptor protein ShcD as upregulated in triple‐negative breast cancer and found its expression to be correlated with reduced patient survival and increased invasion in cell models. Using a proteomic screen, we identified novel ShcD binding partners involved in EGFR signaling pathways.
Hayley R. Lau+11 more
wiley +1 more source
Dual targeting of AKT and mTOR using MK2206 and RAD001 reduces tumor burden in an intracardiac colon cancer circulating tumor cell xenotransplantation model. Analysis of AKT isoform‐specific knockdowns in CTC‐MCC‐41 reveals differentially regulated proteins and phospho‐proteins by liquid chromatography coupled mass spectrometry. Circulating tumor cells
Daniel J. Smit+19 more
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Interplay of integrins and selectins in metastasis
Here we review the role of integrins and their interplay with selectins in metastasis. The efficacy of integrin‐targeted therapies may be reduced in tumors where metastasis relies heavily on selectins. In certain tumors, integrins and selectins exhibit a synergistic interaction during intraperitoneal dissemination.
Diana Maltseva+2 more
wiley +1 more source
Inhibitor of DNA binding‐1 is a key regulator of cancer cell vasculogenic mimicry
Elevated expression of transcriptional regulator inhibitor of DNA binding 1 (ID1) promoted cancer cell‐mediated vasculogenic mimicry (VM) through regulation of pro‐angiogenic and pro‐cancerous genes (e.g. VE‐cadherin (CDH5), TIE2, MMP9, DKK1). Higher ID1 expression also increased metastases to the lung and the liver.
Emma J. Thompson+11 more
wiley +1 more source
Microglia act as tumor suppressors during brain metastasis colonization but shift to a tumor‐promoting role after melanoma brain metastases form. NF‐κB/RelA signaling emerges as a key driver of this phenotypic shift. Targeting this pathway reprograms microglia into a pro‐inflammatory state, enhancing antitumor immunity and immune checkpoint inhibitor ...
Noam Savion‐Gaiger+2 more
wiley +1 more source
Alectinib resistance in ALK+ NSCLC depends on treatment sequence and EML4‐ALK variants. Variant 1 exhibited off‐target resistance after first‐line treatment, while variant 3 and later lines favored on‐target mutations. Early resistance involved off‐target alterations, like MET and NF2, while on‐target mutations emerged with prolonged therapy.
Jie Hu+11 more
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MIF as an oncogenic driver of low‐heterogeneity melanomas
Shvefel and colleagues identified tumor‐secreted macrophage migration inhibitory factor (MIF) as an upregulated cytokine that mediates immune resistance in melanomas with low‐intratumoral heterogeneity. MIF and its functional paralogue D‐dopachrome tautomerase (D‐DT or MIF‐2) have overlapping but nonidentical signaling functions and are hypothesized to
Thuy T. Tran+4 more
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Ubiquitination of transcription factors in cancer: unveiling therapeutic potential
In cancer, dysregulated ubiquitination of transcription factors contributes to the uncontrolled growth and survival characteristics of tumors. Tumor suppressors are degraded by aberrant ubiquitination, or oncogenic transcription factors gain stability through ubiquitination, thereby promoting tumorigenesis.
Dongha Kim, Hye Jin Nam, Sung Hee Baek
wiley +1 more source