Alpha-Fodrin Antibody IgG/IgA ELISA Kit

SH3 domain-binding glutamic acid-rich-like protein 2 (SH3BGRL2) is a poorly defined member of the SH3BGR gene family with potential roles in cell differentiation and tissue development. Here, we report for the first time that SH3BGRL2 exerts a dual function in breast tumor growth and metastasis. SH3BGRL2 was downregulated in a subset of primary breast tumors, and suppressed breast cancer cell proliferation and colony formation in vitro and xenograft tumor growth in vivo. Strikingly, SH3BGRL2 enhanced breast cancer cell migratory, invasive, and lung metastatic capacity. Mechanistic investigations revealed that SH3BGRL2 interacted with and transcriptionally repressed spectrin alpha, non-erythrocytic 1 (SPTAN1) and spectrin beta, non-erythrocytic 1 (SPTBN1), two important cytoskeletal proteins. Functional rescue assays further demonstrated that depletion of SH3BGRL2 reduced breast cancer cell invasive potential, which was partially rescued by knockdown of SPTAN1 and SPTBN1 using specific small interfering RNA. Moreover, transforming growth factor-beta 1 (TGF-beta 1) transcriptionally activated SH3BGRL2 expression in breast cancer cells through the canonical TGF-beta receptor-Smad pathway. Collectively, these results establish a dual function of SH3BGRL2 in breast cancer growth and metastasis and uncover SH3BGRL2 as a downstream target of the TGF-beta 1 signaling pathway in breast cancer cells.

Membrane-proximal and truncated mutations of colony-stimulating factor 3 receptor (CSF3R) are frequently found in chronic neutrophilic leukemia (CNL) and atypical chronic myeloid leukemia (aCML). However, rearrangement involving CSF3R in hematological neoplasms has not been reported. Here, we report a case of a 21-year-old female diagnosed as aCML with t(1;9)(p34;q34) who presented a CSF3R rearrangement. First, RNA sequencing identified a novel fusion transcript involving exon 17 of CSF3R and exon 50 of non-erythrocytic-1-spectrin-alpha (SPTAN1). Subsequent reverse transcription-polymerase chain reaction (RT-PCR) and bidirectional Sanger sequencing confirmed the in-frame fusion. The breakpoint was located at the C-terminus of CSF3R, suggesting a pattern of truncation mutation of CSF3R. Unexpectedly, the patient failed to achieve a complete hematological response following the SRC kinase inhibitor dasatinib therapy, which has been reported to effectively inhibit truncated forms of CSF3R. The patient accepted allogeneic hematopoietic stem cell transplantation (HSCT) and currently remains in a good state. In conclusion, this report is the first to identify a fusion involving CSF3R and SPTAN1 in aCML with t(1;9)(p34;q34).