Oral squamous cell carcinoma (OSCC), with high potential for metastasis, is the most common malignant tumor of the head and neck. Cancer-associated fibroblasts (CAFs) are the main stromal cells in the microenvironment and aggravate tumor progression. However, whether CAFs are associated with the progression of OSCC remains unknown and the underlying mechanism remains unclear. In the present study, the role of CAFs in mediating OSCC cell migration and invasion was investigated, and the participation of exosomal miR-382-5p in this process was elucidated. In this study, according to the α-SMA staining with immunohistochemistry, 47 OSCC patients were divided into CAFs-rich and CAFs poor groups, and association of CAF density and clinicopathologic features of the OSCC patients were analyzed with Pearson χ 2 test. Transwell assay was used for evaluating cell migration and invasion ability of OSCC cells after being co-cultured with NFs or CAFs, or after added exosomes. qPCR was used to detect the expression of miR-382-5p. Western blot analysis was used to measure the expression of migration and invasion-associated proteins. In the present study, the CAF density in tumor tissues was found to be relevant to OSCC lymph node metastasis and TNM stage. Furthermore, we revealed that miR-382-5p was overexpressed in CAFs compared with that in fibroblasts of adjacent normal tissue and miR-382-5p overexpression was responsible for OSCC cell migration and invasion. Finally, we demonstrated that CAF-derived exosomes transported miR-382-5p to OSCC cells. The present study confirmed a new mechanism of CAF-facilitated OSCC progression and may be beneficial for identifying new cancer therapeutic targets.

Overexpression of CBP60g in Arabidopsis enhanced the defense response, hypersensitivity to abscisic acid and tolerance to drought stress.

No abstract

No abstract

SUMMARYBRI1-ASSOCIATED KINASE 1 (BAK1) was initially identified as a co-receptor of the brassinosteroid (BR) receptor BRI1. Genetic analyses also revealed that BAK1 and its closest homolog BAK1-LIKE 1 (BKK1) regulate a BR-independent cell-death control pathway. The double null mutant bak1 bkk1 displays a salicylic acid-and light-dependent cell-death phenotype even without pathogen invasion. Molecular mechanisms of the spontaneous cell death mediated by BAK1 and BKK1 remain unknown. Here we report our identification of a suppressor of bak1 bkk1 (sbb1-1). Genetic analyses indicated that cell-death symptoms in a weak double mutant, bak1-3 bkk1-1, were completely suppressed by the loss-of-function mutation in SBB1, which encodes a nucleoporin (NUP) 85-like protein. Genetic analyses also demonstrated that individually knocking out three other nucleoporin genes from the SBB1-located sub-complex was also able to rescue the celldeath phenotype of bak1-3 bkk1-1. In addition, a DEAD-box RNA helicase, DRH1, was identified in the same protein complex as SBB1 via a proteomic approach. The drh1 mutation also rescues the cell-death symptoms of bak1-3 bkk1-1. Further analyses indicated that export of poly(A) + RNA was greatly blocked in the nup and drh1 mutants, resulting in accumulation of significant levels of mRNAs in the nuclei. Over-expression of a bacterial NahG gene to inactivate salicylic acid also rescues the cell-death phenotype of bak1-3 bkk1-1. Mutants suppressing cell-death symptoms always showed greatly reduced salicylic acid contents. These results suggest that nucleocytoplasmic trafficking, especially of molecules directly or indirectly involved in endogenous salicylic acid accumulation, is critical in BAK1-and BKK1-mediated cell-death control.

No abstract

No abstract

No abstract