Collagen triple helix repeat containing-1 (CTHRC1), a secreted glycoprotein, is frequently upregulated in human cancers. However, the functional role of CTHRC1 in renal cell carcinoma (RCC) remains unclear. Thus, the aim of this study was to explore the role of CTHRC1 in RCC. Our results demonstrated that CTHRC1 was upregulated in RCC tissues and cell lines. Knockdown of CTHRC1 significantly inhibits the proliferation in RCCs. Furthermore, knockdown of CTHRC1 significantly inhibited the epithelial-to-mesenchymal transition (EMT) process in RCCs, as well as suppressed RCC cell migration and invasion. Mechanistically, knockdown of CTHRC1 inhibited the expression of β-catenin, c-Myc, and cyclin D1 in RCC cells. In conclusion, the results of the present study indicated that CTHRC1 downregulation inhibited proliferation, migration, EMT, and β-catenin expression in RCC cells. Therefore, CTHRC1 may be a potential therapeutic target for the treatment of RCC.

MicroRNAs (miRNAs) have emerged as critical regulators in cancer progression. miR‑613 has been reported as a tumor suppressor gene in many types of human cancers. However, the function of miR‑613 in renal cell carcinoma (RCC) remains unclear. In the present study, the authors aimed to detect the expression of miR‑613 and its function in RCC cell lines. miR‑613 was reported to be significantly downregulated RCC cell lines. Functional analyses demonstrated that overexpression of miR‑613 significantly decreased RCC cell proliferation and invasion. Bioinformatics analysis showed that Frizzled7 (FZD7) was a predicted target of miR‑613, which was verified by dual‑luciferase reporter assay, reverse transcription quantitative‑polymerase chain reaction and western blot analysis. Restoration of FZD7 significantly reversed the suppressive effects of miR‑613 on RCC cell proliferation and invasion. Taken together, the results of the present study indicated that miR‑613 functions as a tumor suppressor that inhibits RCC cell proliferation and invasion by targeting and inhibiting FZD7, providing novel insight into RCC pathogenesis and a potential therapeutic target for RCC.

Background: Wilms tumor (WT) is an embryonic malignant tumor, and its related mechanism is still unclear. microRNA (miR), as a short-chain non-coding RNA, has low expression in various tumors. In this study, WT differential miR was screened by multi-chip in GEO database and its mechanism was explored to provide potential therapeutic targets and ideas for clinic. Methods: We logged into GEO database and downloaded GSE57370 and GSE48137 chip matrix files to analyze potential differences in miR. TargetScan, miRDB, miRTarBase and starBase were applied to predict the target genes of miR with significant differences. qRT-PCR was applied to determine the expression of miR-30d and Sox4 in WT tissue and cell line (G401). The interaction of miR-30d with Sox4 was confirmed by qRT-PCR, Western blot and luciferase assay, respectively. CCK-8, Transwell and flow cytometry were applied to determine the proliferation, invasion, migration and apoptosis of cells. Results: We found that miR-30d was low expressed in two chips. qRT-PCR showed that miR-30d was down-regulated and SOX4 was up-regulated in WT tissues and cells. The online target gene prediction software showed there was a targeted binding site between Sox4 and miR-30d. Sox4 was negatively controlled by miR-30d. Subsequent studies found that over-expression of miR-30d inhibited the proliferation, invasion, migration and induced apoptosis of C64 and WiT49 cells. In addition, Sox4 could reverse the proliferation, invasion and migration of C64 and WiT49 induced by miR-30d and induce apoptosis. Conclusion: miR-30d is poorly expressed in WT and can induce apoptosis and inhibit proliferation, invasion and migration by mediating Sox4.

SUMMARY Using computer-aided engineering (CAE) in the concept design stage of automobiles has become a hotspot in human factor engineering research. Based on human musculoskeletal biomechanical computational software, a seated human-body musculoskeletal model was built to describe the natural sitting posture of a driver. The interaction between the driver and car in various combinations of seat-pan/back-rest inclination angles was analyzed using an inverse-dynamics approach. In order to find out the “most comfortable” driving posture of the seat-pan/back-rest, the effect of seat-pan/back-rest inclination angles on the muscle activity degree, and the intradiscal L4-L5 compression force were investigated. The results showed that a much larger back-rest inclination angle, approximately 15°, and a slight backward seat-pan, about 7°, may relieve muscle fatigue and provide more comfort while driving. Subsequently, according to the findings above, a preliminary driving-comfort function was constructed.