Glycosylation plays an important role in the genesis of various cancers. The inhibition of glycosylation disturbs the protein folding machinery, causing the accumulation of unfolded proteins in the cell endoplasmic reticulum (ER) and inducing ER stress. Tunicamycin (TM) is an inhibitor of glycosylation that has shown marked antitumor activity. In this study, we investigated the effect of TM on the tumorigenesis of head and neck cancer cells. The effects of TM on cell proliferation, colony formation and tumorsphere formation in vitro and tumorigenicity in vivo were investigated in head and neck cancer cells. ER stress was determined by the evaluation of PERK, PDI, IRE1-α, BIP, Ero1-Lα and calnexin expression using western blotting and immunofluorescence. We found that TM inhibited colony formation and tumorsphere formation of head and neck cancer cells in vitro and suppressed tumor growth in vivo. After incubation with TM, the expression of the cancer stem cell markers CD44 and Bmi-1 was reduced, and the expression of the ER stress markers BIP, Ero1-Lα and calnexin was elevated. Moreover, the EGFR signaling pathway was inhibited, and nonglycosylated EGFR degradation was accelerated with TM treatment. Our results suggest that inhibition of glycosylation by TM may be a novel treatment strategy for use with HNSCC patients. AJTR Copyright © 2020.AIMS In previous studies, numerous differential lncRNAs were identified via RNA-sequencing. In this dysregulated lncRNAs, lincRNA02471 attracted our attention due to its highest fold change. The aims of our study mainly focused on the function and mechanism of lincRNA02471 in papillary thyroid cancer. MATERIALS AND METHODS Overexpression and knockdown vectors were constructed to investigate the function of lincRNA02471. Proliferation, apoptosis, invasion and EMT were performed to assess the function of lincRNA02471. Dual-luciferase reporter assay was performed to explore the relationship between lincRNA02471 and miR-758. RESULTS We found that lincRNA02471 was manifestly upregulated in papillary cancer tissues. Overexpression of lincRNA02471 significantly promoted the cell proliferation, invasion and inhibited cell apoptosis. Knockdown of lincRNA02471 inhibited the cancer development. We also found that lincRNA02471 negatively regulate miR-758 in papillary thyroid cancer. miR-758 can restore the effect of lincRNA02471. Besides, we identified that HIPK3 was the direct target of miR-758. CONCLUSION we performed comprehensive study of lincRNA02471 and explore its function and mechanism in papillary thyroid cancer. lincRNA02471 can sponge miR-758 and positively regulate HIPK3 to promote papillary thyroid cancer development. Our study provides new target for clinical treatment and new clues for understanding the molecular mechanism of cancer development. this website AJTR Copyright © 2020.The clinical efficacy of PD-1/PD-L1 monoclonal antibodies (mAbs) in triple-negative breast cancer (TNBC) is unsatisfactory. Immunotherapy combined with chemotherapy shows good therapeutic potential. Preclinical and clinical studies have shown that metronomic chemotherapy may stimulate anticancer immune responses. We aimed to verify whether metronomic paclitaxel (PTX, TAX) treatment can improve the efficacy of a PD-1 mAb in a TNBC mouse model and to explore the potential mechanism. After constructing the TNBC mouse model and treating with PD-1 mAb, metronomic PTX chemotherapy or combined therapy, the differences in the efficacy of each treatment group were compared and analyzed. Our findings suggested that the combination of metronomic PTX chemotherapy and PD-1 mAb produces a potent antitumor effect. Further experiments demonstrated that metronomic PTX chemotherapy changed the immune cell population in tumor tissues. These data suggest that metronomic PTX improves the efficacy of the PD-1 mAb in TNBC by transforming the tumor immune microenvironment, and these results provide strong evidence for the use of this treatment in TNBC patients in the future. AJTR Copyright © 2020.We investigated the role of insufficiency of the active form of vitamin D, 1,25-dihydroxyvitamin D [1,25(OH)2D] in age-related bone loss. We employed mice with heterozygous deletion of Cyp27b1, the gene encoding the enzyme that synthesizes 1,25(OH)2D, as a model for 1,25(OH)2D insufficiency and compared the phenotype of lumber vertebrae from 3-, 9- and 18-month-old Cyp27b1+/- mice and their wild-type littermates. We found that in wild-type mice, bone mineral density, bone volume, and Cyp27b1 protein expression levels decreased progressively with age, accompanied by declining osteoblastic bone formation and increasing osteoclastic bone resorption, however these age-related skeletal alterations were more severe in Cyp27b1+/- mice which had significantly lower serum 1,25(OH)2D levels. We then assessed the effect of 1,25(OH)2D haploinsufficiency on oxidative stress and DNA damage, cell senescence and senescence-associated secretory phenotype (SASP) in 9-month-old wild-type and Cyp27b1+/- mice. Our results demonstrated that, in Cyp27b1+/- mice compared with their wild-type littermates, the parameters of oxidative stress and DNA damage were significantly increased, whereas the expression levels of antioxidant enzymes were significantly down-regulated; the percentage of senescent osteocytes and bone marrow mesenchymal stem cells, and the expression levels of SASP molecules and p16, p19 and p53 proteins were all significantly increased in bone tissues. Taken together, the results of this study indicate that 1,25(OH)2D insufficiency accelerates age-related bone loss by increasing oxidative stress and DNA damage, inducing bone cell senescence and SASP, and subsequently inhibiting osteoblastic bone formation while stimulating osteoclastic bone resorption. AJTR Copyright © 2020.Chronic obstructive pulmonary disease (COPD) is a devastating and common respiratory disease characterized by chronic inflammation and progressive airway remodeling. Ginsenoside Rg1 (GRg1), a major active component of Panax ginseng, has been found to possess beneficial properties against acute lung injury and respiratory diseases. However, the effects of GRg1 on airway remodeling in COPD remain unclear. In this study, we aimed to investigate the potential protective effects of GRg1 on airway remodeling induced by cigarette smoke (CS) and the underlying mechanism. A rat model of COPD was established in which the animals were subjected to CS and GRg1 daily for 12 weeks. Subsequently, we evaluated lung function, inflammatory responses, along with airway remodeling and associated signaling factors. GRg1 treatment was found to improve pulmonary function, reduce airway collagen volume fraction, and markedly reduce the expression of IL-6, TNF-α, α-SMA, and collagen I. Moreover, GRg1 treatment decreased the expression of TGF-β1, TGF-βR1, and phosphorylated-Smad3.