Volume 102 Issue 11, November 2022

Proteomics plays a vital role in biomedical research in the post-genomic era. With the technological revolution and emerging computational tools, proteomic methodology has evolved rapidly in the past decade and shed light on solving complicated biomedical problems. Thus, this mini-review summarizes existing and emerging high-throughput proteomics methodologies, including mass spectrometry, protein pathway array, next-generation tissue microarrays, single-cell proteomics, single-molecule proteomics, Luminex, Simoa and OLINK Proteomics.

The authors identified a novel long non-coding RNA (lncRNA), DLGAP1-AS1, that exhibits oncogenic. properties in non-small-cell lung cancer (NSCLC). DLGAP1-AS1 was highly expressed in NSCLC. tissues and cells. Inhibition of lncRNA DLGAP1-AS1 suppressed NSCLC progression both in vitro and. in vivo via the miR-193a-5p/denticleless protein homolog (DTL) axis. This novel regulatory network. provides a potential therapeutic strategy for NSCLC.

Hyperglycemia induces endoplasmic reticulum stress and increases expression of MAPK10, and 4-phenylbutyric treatment and the knockdown of MAPK10 both alleviate hyperglycaemia-induced myocardial dysfunction, respectively. Therefore, the present study sheds new light on the novel role of MAPK10 in hyperglycemia-induced myocardial dysfunction in db/db mice.

Levels of E3 ligase FBXW7 are depressed in radioresistant cells. Overexpression of FBXW7 represses proliferation and colony formation and increases γ-H2AX-positive foci in cultured cells. Overexpression of FBXW7 increases ubiquitination levels and reduces the stability of SOX9, which binds to the CDKN1A promoter to inhibit expression. The authors conclude that FBXW7 inhibits tumorigenesis and apoptosis and enhances radiosensitivity of NSCLC cells via SOX9/CDKN1A.

The replacement and desmoplastic histopathological growth patterns (HGP) were studied in patients with uveal melanoma liver metastases (MUM). L1CAM and laminin vascular network were detected at the advancing front of the high-risk replacement HGP but not in the more prognostically favorable desmoplastic HGP. Any percentage of replacement HGP (rHGP), predominant rHGP, or pure rHGP in MUM had a significant adverse effect on metastasis-specific overall survival (p = 0.038; (p = 0.0058); p = 0.0064

Nobiletin (NOB) has significant neuroprotective effects on retinal ganglion cells (RGCs) in glaucomatous neurodegeneration, including reducing RGC apoptosis and oxidative stress, partially restoring RGC dysfunction, further enhancing Nrf2/HO-1 pathway in RGCs, and attenuating Müller glial activation. These effects do not depend on lowering intraocular pressure. Intervention to enhance activation of Nrf2/HO-1 pathway are viable therapies for glaucoma.

This study presents a novel perspective on the influences of the microbiome-cancer axis during tumor development and treatment, in a syngeneic, immunocompetent mammary tumor mouse model. The findings define substantial remodeling of the gut microbiome and changes in the intestinal immune network in response to the orally administered therapeutic Hedgehog inhibitor, Vismodegib, and highlight the dynamic shifts in the abundance of pro- and anti-inflammatory gut microbes during tumor progression and in response to Hedgehog blockade.

Lymph node metastasis (LNM) worsens the prognosis of nasopharyngeal cancer (NPC) patients. Thus, bioinformatic analysis was used to determine a key gene, the tyrosine-kinase receptor KITLG, that might play a critical rols in the LNM of NPC. The suppression of KITLG inhibits the proliferation, invasion, and metastasis of NPC cells via the JAK/STAT signaling pathway.

The levels of m6A and WTAP are elevated in the CD4+ T cells of tolerant kidney transplant recipients. In naïve CD4+ T cells from kidney transplant recipients with immune rejection, WTAP is highly expressed and facilitates Foxo1 transcription by enhancing m6A modification of Foxo1 mRNA in the CDS region, which enhances Foxo1-mediated Foxp3 transcription and subsequent Treg cell differentiation and function.

GPM6A expression is markedly suppressed in hepatocellular carcinoma and suppresses proliferation and migration of hepatoma cells. Moreover, its low expression is most likely attributed to upregulated miRNA-96-5p but not gene mutation or changes in methylation. These findings indicate that GPM6A may function as an inhibitory gene in chronic information, fibrosis and oncogenic transformation.