Anti-XIAP (C-terminal) polyclonal antibody

Although there are several studies, biological function and therapeutic potential of miR-17-5p in breast cancer carcinogenesis remains muchly elusive. Specifically, its interaction with several cancer-associated genes remains unexplored in breast cancer. Here, we aimed to demonstrate the biological function and therapeutic potential of miR-17-5p in breast cancer through determination of the interactions between cancer-associated genes and miR17-5p. MFC-7 breast cancer cells used in the study and cells were transfected with miR-17-5p miRNA mimics to ectopically overexpress miR-17-5p. MiR-17-5p expression levels and expression changes of cancer-associated genes were determined by using qPCR method. Expression levels of miR-17-5p were significantly enhanced following 72 h of mimic transfections as compared to scrambled control and blank control. Overexpression of miR-17-5p led to differential expression of several cancer-associated genes. Notably, BECN, CDKN2B and AIFM genes were significantly altered. Although not significant, expression levels of BAX, BCLXL, VIM, BCL2, MTOR, RB1, AKT1, XIAP, P53, and PTEN genes were found to be slightly elevated whereas expression levels of BCL-2, VIM and AKT1 were found to be decreased. Results of the present study indicate that miR-17-5p can act as both tumor suppressor and tumor promoter oncomiR in breast cancer.

Introduction: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL or Apo2L) is a member of the Tumor Necrosis Factor (TNF) superfamily, which stimulates apoptosis in a wide range of cancer cells through binding to Death Receptors 4 and 5 (DR4/5). Nevertheless, TRAIL has noticeable anti-cancer abilities; some cancer cells acquire resistance to TRAIL, and consequently, its potential for inducing apoptosis in target cells is strongly diminished. Acute lymphoblastic leukemia MOLT-4 cell line is one of the most resistant cells to TRAIL that developed resistance to TRAIL through different pathways. TRAIL plus kaempferol was used to eliminate the resistance of the MOLT-4 cells to TRAIL. Materials and Methods: Firstly, IC50 for kaempferol (95 mu M) was determined by using the MTT assay. Secondly, the viability of the MOLT-4 cells was assayed by FACS after Annexin V/PI staining, following treatment with TRAIL (50 and 100nM) and kaempferol (95 mu M) alone and in combination. Finally, the expression levels of the candidate genes involved in resistance to TRAIL were assayed by real-time PCR technique. Results: Kaempferol plus TRAIL induced apoptosis robustly in MOLT-4 cells at 12, 24 and 48 hours after treatment. Additionally, it was found that kaempferol could inhibit the expression of c-FLIP, cIAP1/2, FGF-8 and VEGF-beta, and conversely augment the expression of DR4/5 in MOLT-4 cells. Conclusion: It is suggested that co-treatment of MOLT-4 cells with TRAIL plus kaempferol is a practical and attractive approach to eliminate cancers' resistance to TRAIL by inhibition of the intracellular anti-apoptotic proteins, upregulation of DR4/5 and also by suppression of the VEGF-beta (VEGFB) and FGF-8 expressions.