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The cover shows DSS1 and PCID2 immunohistochemistry results in normal breast tissue (left), ductal carcinoma in situ (center), and invasive ductal carcinoma (right). DSS1 expression tended to be higher with increased malignancy, whereas PCID2 was always expressed. For more information, see the paper by Gondo et al, p 1048 this issue.
This study describes a methodology to assess the microenvironment in sparse tissue samples. Deep learning, multiplex immunohistochemistry, and mathematical image processing techniques were incorporated to quantify lymphocytes, macrophages, and capillaries in kidney transplant biopsies of delayed graft function patients. The quantitative results were used to assess correlations with development of interstitial fibrosis and tubular atrophy.
The expression of TRIM27 in MRL/lpr mice and human renal glomerular endothelial cells cultured in vitro is significantly enhanced. Downregulating the expression of TRIM27 inhibits the loss of glycocalyx and damage to endothelial cells through the FoxO1 pathway. In addition, inhibition of the protein kinase B (Akt) pathway can reduce the damage by mediating the expression of TRIM27.
MicroRNA-432-5p expression in osteosarcoma cells regulates sprouting and intussusceptive angiogenesis by targeting PDGFB genes. MicroRNA-432-5p/PDGFB signaling can be targeted to treat angiogenesis in osteosarcoma along with other strategies which will further strengthen the effectiveness of antiangiogenic therapy.
miR-181b inhibits HUVEC migration and tube formation in vitro, and suppresses perfusion recovery in a hindlimb ischemia animal model and in a capillary density assay. Cellular communication network factor 1 (CCN1) is a direct target of miR-181b. miR-181b suppresses angiogenesis at least in part by targeting CCN1 to inhibit the AMPK signaling pathway.
Reduced pS6 correlates with sensitivity to MEK inhibition in colorectal cancer organoids as well as cell lines. This study shows the potential applicability of MEK inhibitors for a subset of colorectal cancer patients with RAS/BRAF mutation by using the change in pS6 levels as a predictive diagnostic marker.
Depletion of DSS1 and PCID2, components of the TREX-2 complex, increases chemosensitivity via BRCA2-independent DNA damage in breast carcinomas. Unlike PCID2, DSS1 is not highly expressed in normal breast tissues; therefore, DSS1 depletion confers a druggable trait, providing an approach for treating breast carcinomas independent of BRCA2 mutations.
The m6A modification level of LncRNA FENDRR is elevated in endometrioid endometrial carcinoma (EEC) cells and the abundant m6A modification promotes FENDRR degradation via recruiting the m6A binding protein YTHDF2. Subsequently, the downregulation of FENDRR resulted in the accumulation of SOX4 protein, thus boosting the proliferation of EEC cells.
Long noncoding RNAs GAS5 activates the HIF1A/VEGF pathway by binding to TAF15 (a component of RNA polymerase II), resulting in accelerated wound healing in diabetic foot ulcers. These findings may provide a theoretical basis for clinical treatment.
The therapeutic effects of CP-25 on experimental Sjögren’s syndrome has been shown to be associated with the inhibition of the JAK1-STAT1/2-CXCL13 signaling pathway in HSGEC, which impedes the migration of B cells into the salivary gland. The study provides an experimental foundation for CP-25 as a potential drug in the treatment of human autoimmune disorder, Sjögren’s syndrome.
Using a mouse model of fatty liver and correlation with histopathologic and biochemical parameters, the authors show that hepatic steatosis can be accurately assessed by surface color spectrophotometry using a portable, commercially available, hand-held spectrophotometer device. This technique could be useful in the setting of organ procurement.