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Abstract CDKL1 is a cyclin-dependent kinase-like kinase that is highly expressed in diverse types of cancer cells. However, the role of CDKL1 in the chemoresistance of oral squamous cell carcinoma (OSCC) remains largely undefined. Here, we explored the role of CDKL1 in the chemoresistance of the human OSCC cell line CAL27 to hydroxycamptothecin (HCPT). Real-time quantitative polymerase chain reaction and western blotting revealed that exposure of CAL27 cells to HCPT led to a marked increase in the expression of CDKL1 at the mRNA and protein levels. Knockdown of CDKL1 significantly suppressed cell proliferation and induced cell cycle G0/G1 phase arrest in CAL27 cells based on the results of MTT and flow cytometry assays, respectively. CAL27 cells displayed attenuated biological activity of the cell population. After treatment with HCPT, whereas CDKL1 overexpression increased the resistance to HCPT of the remaining cells. Moreover, the western blot showed that the expression of cleaved-caspase 3 and phosphorylated ataxia telangiectasia mutated proteins was upregulated by HCPT treatment in CAL27 cells. Furthermore, CDKL1 overexpression partially reversed the inhibitory effects of HCPT in CAL27 cells. These results suggest that CDKL1 overexpression decreased the chemosensitivity of OSCC cells to HCPT, indicating a potential strategic approach for reversing the HCPT resistance in human OSCC. Highlights • The role of CDKL1 in the chemoresistance of the human OSCC cell line CAL27 to hydroxycamptothecin (HCPT). • Exposure of CAL27 cells to HCPT led to a marked increase in the expression of CDKL1. • Attenuated proliferation activity after treatment with HCPT. • CDKL1 overexpression increased the resistance to HCPT of the remaining cells. • CDKL1 overexpression partially reversed the inhibitory effects of HCPT in CAL27 cells. • CDKL1 overexpression decreased the chemosensitivity of OSCC cells to HCPT. [ABSTRACT FROM AUTHOR]

Temporomandibular joint osteoarthritis (TMJ OA) is an important subtype of temporomandibular disorders (TMD). Articular cartilage destruction is considered a common pathological feature of TMJ OA, which is reported to be mainly induced by chondrocyte apoptosis. Synovial sterile inflammation is an initial factor of TMJ OA-associated articular cartilage destruction. Therefore, determining the mechanism of synovial membrane inflammation-induced articular cartilage destruction in TMJ OA is important for the TMJ OA therapy. In this study, we detected the function of synoviocytes in chondrocyte apoptosis under lipopolysaccharide (LPS)-induced inflammatory conditions and explored the underlying mechanism. We found that synoviocytes in inflammatory conditions facilitated LPS-induced chondrocytes apoptosis by secreting increased Tumor Necrosis Factor α (TNF-α), which was induced by long non-coding RNA plasmacytoma variant translocation 1 (PVT1) upregulation. PVT1 served as a competing endogenous RNA that sponged the microRNA miR-211-3p and prevented the inhibition of TNF-α expression. In conclusion, our in vitro study revealed that PVT1 has a previously unknown role in chondrocyte apoptosis, which may also be a mechanism underlying synoviocyte involvement in TMJ OA. • LPS-stimulated synoviocytes aggravate chondrocytes apoptosis. • PVT1 participates in synoviocytes cells-aggravated chondrocytes apoptosis. • PVT1 upregulates TNF-α through sponging miR-211-3p. [ABSTRACT FROM AUTHOR]

Gene fusion is caused by the linkage of previously separate genes or sequences. Recently, an increasing number of novel fusion genes have been identified and associated with tumor progression, and several of them have been suggested as promising targets for tumor therapy. However, there are hardly any studies reporting the association of fusion genes with the progression of oral squamous cell carcinoma (OSCC). In this study, we identified a total of 11 fused genes in OSCC cells. We further analyzed the structure of one fused gene, TRIM52-RACK1, and detected its function in tumor progression in vitro. We found that TRIM52-RACK1 was caused by a deletion of 181,257,187-181,247,386 at 5q35.3 and it promoted OSCC cell proliferation, migration, and invasion. Therefore, TRIM52-RACK1 can be a promising target for tumor therapy in OSCC. • Eleven fused genes were found in OSCC cells. • Fused gene, TRIM-RACK1, was caused by the deletion of 181,257,187-181,247,386 at 5q35.3. • TRIM52-RACK1 promotes OSCC cells proliferation, migration and invasion. [ABSTRACT FROM AUTHOR]

Based on the high self-renewal ability and osteoblastic differentiation capacity, dental pulp stem cells (DPSCs) are suggested to be promising cell source for osteogenesis. Therefore, illustrating the mechanism of osteoblastic differentiation of DPSCs is required. This current study aims to illustrate the role and mechanism of Sp1 in regulating osteoblastic differentiation of DPSCs. In this study, we downregulated Sp1 in DPSCs and evaluated the osteoblastic differentiation by measuring Runx2 and OCN expression with Western blot analysis and by Alizarin red staining. Furthermore, we investigated the mechanism of Sp1 regulating noggin with Firefly luciferase reporter gene assay and ChIP assay, and correspondingly evaluated the function of noggin in Sp1-regulated osteoblastic differentiation of DPSCs. We found that knockdown of Sp1 inhibits the expression of ALP, Runx2, COL1A1 and OCN, and decreases ALP staining, Alizarin red staining. Sp1 binds to noggin promoter and inhibits noggin expression, thus correspondingly regulates DPSCs osteoblastic differentiation. In conclusion, our study revealed that Sp1 regulates DPSCs osteoblastic differentiation through noggin and that Sp1/noggin can provide new perspective for enhancing DPSCs osteogenesis. • Sp1 promotes osteoblastic differentiation of DPSCs. • Sp1 regulates osteoblastic differentiation of DPSCs by downregulating noggin. • Sp1 regulating noggin through modulating noggin promoter activity. [ABSTRACT FROM AUTHOR]