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In conclusion, we show that MCF-7 cells cause osteosclerotic bone metastases and that Neu enhances this capacity of MCF-7 cells.
The results support the conclusion that the MCF-7 cell line is heterogeneous and that the selection conditions allow the growth of pre-existing phenotypes.
Based on these, we concluded that MMP‐7 is a potential marker to identify patients with metastatic prostate cancer.
The results revealed that the MCF-7 cells were stiffer than M231 cells, implying that the M231 cells possessed higher metastatic potential.
Most of the genes changed may promote the metastasis of MCF-7 cells while the others may inhibit metastasis.
These results showed that CMDB7 inhibits the mitogenic effect of growth factors released from MCF-7 and MCF-7ras cells and suppresses tumor growth in the MCF-7ras model.
RAPTA-T shows a lack of membrane accumulation on the non-invasive MCF-7 cells, which correlates well with its selective anti-metastatic properties on invasive cell lines.
The results indicated that the MCF-7 cells possessed a tumor-associated antigen to which many patients with breast carcinoma are sensitized.
These data thus showed that MCF-7 sublines differed at both the genomic and phenotypic levels. The analysis of CGH profiles of the parent subline and its three subclones supported the heteroclonal nature of MCF-7 cells.
These observations suggest that MCF-7/ADR cells might have originated in a selection of ductal infiltrating carcinoma cells, which were present among the original MCF-7 cell population.

Related Questions

What are the molecular mechanisms underlying metastatic progression in cancer?5 answersMetastatic progression in cancer is driven by various molecular mechanisms. Recent advancements in cancer biology research have shed light on some of these mechanisms. Genetics and epigenetics play a crucial role in regulating metastatic events. Proteins such as MT4-MMP contribute to tumor development and metastasis by triggering molecular mechanisms involved in tumor cell migration, invasiveness, and proliferation. Additionally, the tumor microenvironment, including the extrinsic traits, integrins, chemokines, and exosomes, also play a role in metastatic initiation, progression, and colonization. Chromosomal instability and micronuclear rupture have been identified as key events in aggressive cancers, leading to genomic rearrangements and activation of inflammatory pathways that promote metastatic progression. Understanding these molecular mechanisms is crucial for developing effective therapeutic interventions to prevent or delay metastasis.
What is the IC50 of doxorubicin in MCF7?4 answersThe IC50 of doxorubicin in MCF7 cells was found to be 3.73 µM.
Is CTCFL relate to NSCLC or metastasis?5 answersCTCFL, also known as NEFL, is related to non-small cell lung cancer (NSCLC) and metastasis. Studies have shown that NEFL expression is associated with decreased lymph node metastases and favorable prognosis in NSCLC patients. Knocked-down of NEFL enhances the invasion and migration of NSCLC cells, while NEFL overexpression suppresses invasion and migration in vitro. NEFL downregulation is associated with promoter methylation, and NEFL expression can be restored after treatment with 5-Aza-dC. NEFL inhibits the NF-κB pathway, thereby suppressing the expression of uPA and decreasing NSCLC invasiveness and migration. Additionally, the EMT phenotype of circulating tumor cells (CTCs) in the peripheral blood of NSCLC patients is associated with distant metastasis. E+/M+ CTCs and M+ CTCs have been identified as potential predictors of distant metastasis in NSCLC patients.
What are the correlation between MCF7 and E-cadherin and N-cadherin?3 answersMCF7 cells are known to express E-cadherin and N-cadherin. The switch between E-cadherin and N-cadherin expression has been implicated in breast cancer progression, spread, and metastasis. Cancer-associated fibroblasts (CAFs) exert a physical force on cancer cells through a heterophilic adhesion involving N-cadherin at the CAF membrane and E-cadherin at the cancer cell membrane. E-cadherin and N-cadherin can form heterotypic connections in physiological and disease environments. In a knock-in mouse model, the presence of N-cadherin in alveolar epithelial cells of the mammary gland induced constitutively active fibroblast growth factor signaling and a precocious involution, leading to fibrosis and cyst formation. The upregulation of N-cadherin and downregulation of E-cadherin are hallmarks of epithelial-to-mesenchymal transition (EMT), which enhances metastasis and chemoresistance in cancer.
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