CS1 promotes multiple myeloma cell adhesion, clonogenic growth, and tumorigenicity via c-maf-mediated interactions with bone marrow stromal cells.
Level 5 - mechanism / opinion, no new human data
Preclinical in vitro and animal research without human clinical trial data
PubMed 19196658 · doi:10.1182/blood-2008-10-183772
What was done
Investigators evaluated the functional role of CS1 in multiple myeloma (MM) cell lines and mouse models. Lentiviral siRNA knockdown of CS1 was used to measure effects on ERK1/2, AKT, and STAT3 signaling, apoptosis induction upon serum deprivation, and in vivo tumor growth and survival in mice. CS1 overexpression was also examined for its effects on MM cell adhesion to bone marrow stromal cells (BMSCs), colony formation, c-maf downstream targets (cyclin D2, integrin beta7/alphaE), and VEGF-induced bone marrow angiogenesis.
What was found
The abstract reports no numerical values. Directionally, CS1 knockdown decreased phosphorylation of ERK1/2, AKT, and STAT3, accelerated caspase, PARP, BNIP3, and BIK activation during serum starvation, delayed tumor development, and extended survival in mice. CS1 overexpression increased myeloma adhesion to BMSCs, colony formation in semisolid culture, cyclin D2-dependent proliferation, integrin beta7/alphaE-mediated adhesion, and in vivo angiogenesis.
Why it matters
This study provided preclinical rationale and mechanistic context for targeting CS1 in multiple myeloma therapeutic development.
Limits
The study is entirely preclinical (in vitro cell culture and mouse models) and reports no quantitative data or sample sizes in the abstract. Crucially, the PubMed record designates this article as a Retracted Publication, indicating that its underlying data and conclusions cannot be considered reliable.
Cited by
- context A multiple myeloma study from the Dana-Farber Cancer Institute published in Blood contained duplicated/manipulated images where day 1 control group images were reused for day 16 intervention groups to claim tumor suppression.