Subcutaneous injection model and tail vein injection model showed that forced expression of MEG2 in HCCLM3 decreased the growth and lung metastasis of HCCLM3 cells in nude mice.
CPEB2KO, but not wild-type cells produced lung colonies upon intravenous injection and subcutaneous tumors and spontaneous lung metastases upon implantation at mammary sites in NOD/SCID/IL2Rϒ-null mice, identified with HLA immunostaining.
We stained tissue microarrays from resected primary lung cancer (n = 665) and pulmonary metastases (n = 425) for CK7, CK20, CDX2, CK5, p40, p63, TTF-1, napsin A, GATA3, and PAX8 to systematically assess the diagnostic value of these markers.
In addition, the in vivo mouse xenograft model showed that overexpression of miR-615-3p inhibited NSCLC growth and lung metastasis, whereas decreased expression of miR-615-3p caused an opposite outcome.
Moreover, regulators such as TFAP2C, GTF2I and LMO4 were found to have potential prognostic value for lung metastasis free (LMF) survival of breast cancer.
In mouse models, administration of either APR-246 or 2aG4 reduced metastasis of TNBC cells to the lungs; a combination of the two diminished lung metastasis to the same extent as either agent alone.
BAP31 knockdown suppressed cell proliferation, clonogenic ability and metastasis-associated traits in vitro, as well as carcinogenesis and pulmonary metastasis in vivo.
Inhalation of phosphatidylserine coated liposome loaded with STING agonist cyclic guanosine monophosphate-adenosine monophosphate (NP-cGAMP) in mouse models of lung metastases enables rapid distribution of NP-cGAMP to both lungs and subsequent uptake by APCs without causing immunopathology.
In <i>in vivo</i> murine models, anti-KLRG1 antibody monotherapy in the 4T1 breast cancer model reduced lung metastases (decreased lung weights p=0.04; decreased nodule count p=0.002), while anti-KLRG1 + anti-PD-1 combination therapy in the MC38 colon cancer and B16F10 melanoma models produced synergistic benefit greater than anti-PD-1 alone for tumor volume (MC38 p=0.01; B16F10 p=0.007) and survival (MC38 p=0.02; B16F10 p=0.002).
This phenomenon was associated with PMEPA1 KO-mediated downregulation of the key proangiogenic factors vascular endothelial growth factor alpha (VEGFA) and interleukin-8 (IL8) that are essential for in vivo but not in vitro growing cells and are also substantial for initiation of lung metastasis.
Importantly, we showed that NDRG1 was essential in MORC2-mediated promotion of CRC cell migration and invasion in vitro, as well as lung metastasis of CRC cells in vivo.
We stained tissue microarrays from resected primary lung cancer (n = 665) and pulmonary metastases (n = 425) for CK7, CK20, CDX2, CK5, p40, p63, TTF-1, napsin A, GATA3, and PAX8 to systematically assess the diagnostic value of these markers.
Our study reveals that MDSCs derived by CXCL17 contribute to the establishment of a lung metastatic niche by PDGF-BB secretion and provide a rationale for development of CXCL17 or PDGF-BB antagonists to inhibit or prevent lung metastasis in cases of breast cancer.
Although PCDH7 was recently shown to promote transformation and facilitate brain metastasis in lung and breast cancers, decreased PCDH7 expression has also been documented in colorectal, gastric, and invasive bladder cancers.
A lung metastasis model of mice HCC was constructed to test the potential effect of SLC46A3 on cancer metastasis and a subcutaneous xenografted tumor mice model was designed to verify the effect of SLC46A3 on the resistance of HCC cell lines to sorafenib.