Rabbit Anti-Human POLA1 (a.a. 1231-1350) Polyclonal antibody

MiR-206 acts as a potential tumor suppressor during carcinogenesis and a regulatory factor in osteoblasts differentiation, but its modulatory mechanism remains unclear. In this study, we used a quantitative proteomics method, difference gel electrophoresis (DIGE), to profile the protein variation in A549 lung cancer cells with and without miR-206 transfection. We identified a total of 17 differently expressed proteins including 5 up-regulated and 12 down-regulated proteins affected by miR-206 in A549 cells. We further constructed a protein network linked 17 differently expressed proteins with 106 computationally predicted miR-206 targets, and identified 8 "hub" genes (CALR, CTSD, ENO1, HSPA5, CDC42, HSPD1, POLA1, and SMARCA4) within the network, which may represent important miR-206 functional gene targets. In conclusion, in this study, we identified several candidate functional target genes for miR-206, which is helpful to further explore its mechanisms during carcinogenesis and osteogenesis, and we also proposed a novel proteomic strategy to identify functionally important gene targets for microRNA.

Malignant proliferation is the fundamental trait of tumor cells. The initiation of DNA replication represents a key process for cell proliferation, and has a marked impact on tumorigenesis and progression. Here we report that Sine oculis homeobox homolog 1 (SIX1) functions as a master regulator in DNA replication of cervical cancer cells. The expression of SIX1 was induced by the E7 oncoprotein of human papillomaviruses in cervical intraepithelial neoplasia and cervical cancer. The increase of SIX1 expression resulted in the upregulation of multiple genes related to the initiation of DNA replication, including the genes coding for the proteins in minichromosome maintenance complex (MCM2, MCM3, MCM6), DNA polymerase a-primase complex (POLA1, PRIM1, PRIM2), clamp loader (RFC3, RFC4, RFC5), DNA polymerase delta complex (POLD3) and DNA polymerase a complex (POLE2). In line with this, the increase of SIX1 expression enhanced DNA synthesis, accelerated G1 to S phase progression, and promoted the proliferation of cervical cancer cells and the growth of cervical cancer. Consistently, knockdown of SIX1 could hamper DNA synthesis, slow down G1 to S phase progression, and suppress tumor cell proliferation and tumor growth. Importantly, SIX1 could more efficiently promote anchorage-independent cell growth. These results suggest that the increase of SIX1 expression could promote tumorigenesis, progression and invasive growth of cervical cancer by promoting DNA replication, and that targeting SIX1 may have significant therapeutic value in cervical cancer treatment.