Clinical testing of liver metastasis identified BRIP1, NF1, CDH1, RB1, and TP53 mutations pointing to potential therapies including PARP, MEK/RAF, and CDK inhibitors.
Further, we identified that the liver-specific transcription factors FOXA2 and HNF1A can bind to the gained enhancers and activate the liver-specific gene transcription, thereby driving CRC liver metastasis.
Ectopic Corticotropin-Releasing Hormone-Secreting Pancreatic Neuroendocrine Tumor: Excellent Response of Liver Metastases to Peptide Receptor Radionuclide Therapy as Demonstrated by 68Ga-DOTATOC and 18F-FDG PET/CT Imaging.
Functionally, small interfering RNA-mediated TRIM59 depletion inhibited cell proliferation and migration in vitro, while TRIM59 overexpression promoted cell proliferation and migration in vitro and drove tumor growth and liver metastasis in vivo.
As miR-21 and miR-200c were abundantly expressed in both metastatic liver sites and primary lesions, we evaluated Ago2-miR-21 as a candidate biomarker of both active export and cytolysis while Ago2-miR-200c as a biomarker of cytolysis in plasma obtained from colorectal cancer (CRC) patients before treatment and in a series of plasma obtained from CRC patients with liver metastasis who received systemic chemotherapy.
Seventy-two patients with colorectal cancer and 16 patients with colorectal liver metastasis who underwent surgery were included. miR-449a expression in tumor tissue of resected specimen was investigated by real-time polymerase chain reaction and histone deacetylase 1 (HDAC1) expression was examined by immunohistochemistry.
Secreted HDGF promoted tumour angiogenesis, while nuclear HDGF activated GLUT4 and ENO2 expression, followed by an increase in glycolysis in GC cells, which was correlated with subsequent tumour growth and liver metastasis.
The biological effects of TFEB-driven autophagy were investigated in vitro using transwell and wound healing assays and in vivo using liver metastasis and LSL-KrasG12D/Pdx1-Cre mice models.
RP11 positively regulated the migration, invasion and epithelial mesenchymal transition (EMT) of CRC cells in vitro and enhanced liver metastasis in vivo.
The synergistic effect of AP and Tar generates an excellent in vivo tumor targeting and antitumor efficacy of DOX with prolonged survival and minimized side effects, especially for liver metastasis.
Moreover, overexpression of miR-301a-3p could promote the growth of xenograft tumors and liver metastasis in vivo, along with reducing the expressions of DLC-1 and RUNX3.
We demonstrate that gram-negative Escherichia coli pneumonia augments the formation of murine H59 NSCLC liver metastases in C57BL/6 mice through TLR4 activation.