Human FOXP4 blocking peptide

Objectives: Despite improvements in diagnosis and treatment, colorectal cancer (CRC) remains the third most common malignancy, and fourth-leading cause of cancer-related death worldwide, and has a particularly high incidence in Western countries. Recent studies have suggested that long non-coding RNAs (lncRNAs) compose a novel class of regulators of cancer biological processes, such as proliferation, apoptosis and metastasis. Here, we report that lncRNA FOXP4-AS1 acts as a functional oncogene in CRC pathogenesis. Moreover, we have attempted to investigate the effects of FOXP4-AS1 on tumour progression, both in vitro and in vivo. Materials and methods: In this study, bioinformatic analyses and qPCR were performed to investigate FOXP4-AS1 expression in CRC tissue samples and CRC cell lines. We inhibited FOXP4-S1 expression via FOXP4-S1-specific siRNA transfection.Cell proliferation was assessed using cell viability and colony formation assays, as well as by flow cytometry and ethynyl deoxyuridine (Edu) analyses. Apoptosis was assessed using flow cytometry. Animal tumour xenografts were generated, and immunohistochemistry (IHC) was performed to evaluate effects of FOXP4-AS1 on CRC tumour growth in vivo. Results: We found that FOXP4-S1 was up-regulated in CRC tissues and cell lines and that its overexpression positively correlated with advanced pathological stages and larger tumour size. Additionally, we found that FOXP4-AS1 knockdown inhibited cell proliferation and induced apoptosis. Furthermore, FOXP4-AS1 knockdown induced marked increase in number of cells in G0/G1 phase and reduction in number of cells in S phase, in DLD-1, HT-29 and HCT116 cell lines. Consistent with these findings, FOXP4-AS1 silencing inhibited tumour growth in vivo. Conclusion: These findings suggest that FOXP4-AS1 plays a crucial role in CRC progression and may be a new biomarker in patients with CRC.

Objective: Laryngeal cancer is a common malignant tumor in the ENT, of which laryngeal squamous cell carcinoma (LSCC) accounts for more than 90% of laryngeal cancer. The purpose of this study is to investigate the regulatory mechanism of lncRNA SNHG16 in LSCC. Materials and Methods: Real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR) was used to measure mRNA expression. Cell Counting Kit (CCK-8), Transwell and luciferase reporter assays, flow cytometric analysis and Western blot analysis were used to investigate the function of lncRNA SNHG16 in LSCC. Results: SNHG16 expression was increased in LSCC tissues and cells. The abnormal expression of SNHG16 was associated with clinical stage and lymph node metastasis in LSCC patients. In addition, knockdown of SNHG16 restrained cell proliferation, migration and invasion in LSCC. More importantly, SNHG16 acted as a competitive endogenous RNA in LSCC and regulated FOXP4 expression by making miR-877-5p sponge. Further, SNHG16 promoted LSCC progression by interacting with miR-877-5p and FOXP4. Conclusion: LncRNA SNHG16 promotes the progression of LSCC by sponging miR-8775p and upregulating FOXP4.