Diagnosis for Chinese patients with light chain amyloidosis: a scoping review.

Background: Amyloid light chain (AL) amyloidosis is the most common systemic amyloidosis. The objective of this scoping review was to map the available literature on the diagnosis of AL amyloidosis in China.

Materials And Methods: The published academic papers related to the diagnosis of AL amyloidosis were screened from 1 January 2000 to 15 September 2021.

m A Reader YTHDF1-Targeting Engineered Small Extracellular Vesicles for Gastric Cancer Therapy via Epigenetic and Immune Regulation.

N -methyladenosine (m A) modulators decide the fate of m A-modified transcripts and drive cancer development. RNA interference targeting m A modulators promise to be an emerging cancer therapy but is challenging due to its poor tumor targeting and high systematic toxicity. Here engineered small extracellular vesicles (sEVs) with high CD47 expression and cyclic arginine-glycine-aspartic (c(RGDyC)) modification are developed for effective delivery of short interfering RNA against m A reader YTH N6-methyladenosine RNA binding protein 1 (YTHDF1) to treat gastric cancer via epigenetic and immune regulation.

METTL3 preferentially enhances non-mA translation of epigenetic factors and promotes tumourigenesis.

METTL3 encodes the predominant catalytic enzyme to promote mA methylation in nucleus. Recently, accumulating evidence has shown the expression of METTL3 in cytoplasm, but its function is not fully understood. Here we demonstrated an mA-independent mechanism for METTL3 to promote tumour progression.

YTHDF1 Promotes Gastric Carcinogenesis by Controlling Translation of .

N-methyladenosine (mA) is the most prevalent internal RNA modification in mammals that regulates homeostasis and function of modified RNA transcripts. Here, we aimed to investigate the role of YTH mA RNA-binding protein 1 (YTHDF1), a key regulator of mA methylation in gastric cancer tumorigenesis. Multiple bioinformatic analyses of different human cancer databases identified key mA-associated genetic mutations that regulated gastric tumorigenesis.

The m6A reader YTHDF1 promotes ovarian cancer progression via augmenting EIF3C translation.

N 6-Methyladenosine (m6A) is the most abundant RNA modification in mammal mRNAs and increasing evidence suggests the key roles of m6A in human tumorigenesis. However, whether m6A, especially its 'reader' YTHDF1, targets a gene involving in protein translation and thus affects overall protein production in cancer cells is largely unexplored. Here, using multi-omics analysis for ovarian cancer, we identified a novel mechanism involving EIF3C, a subunit of the protein translation initiation factor EIF3, as the direct target of the YTHDF1.

microRNA arm-imbalance in part from complementary targets mediated decay promotes gastric cancer progression.

Strand-selection is the final step of microRNA biogenesis in which functional mature miRNAs are generated from one or both arms of precursor. The preference of strand-selection is diverse during development and tissue formation, however, its pathological effect is still unknown. Here we find that two miRNA arms from the same precursor, miR-574-5p and miR-574-3p, are inversely expressed and play exactly opposite roles in gastric cancer progression.

[Knockdown of YTH N-methyladenosine RNA binding protein 2 (YTHDF2) inhibits proliferation and promotes apoptosis in MGC-803 gastric cancer cells].

Objective To investigate the effect of knockdown of YTH N-methyladenosine RNA binding protein 2 (YTHDF2) on cell proliferation, cell cycle and apoptosis of MGC-803 human gastric cancer cells in vitro. Methods The TCGA database was downloaded from UCSC Cancer Browser and to search for the differential expressions of YTHDF2 mRNA in gastric cancer tissues. Short hairpin RNA (shRNA) targeting YTHDF2 was designed and cloned into lentivirus expression vector pLKO.

The RNA-binding protein QKI5 regulates primary miR-124-1 processing via a distal RNA motif during erythropoiesis.

MicroRNA (miRNA) biogenesis is finely controlled by complex layers of post-transcriptional regulators, including RNA-binding proteins (RBPs). Here, we show that an RBP, QKI5, activates the processing of primary miR-124-1 (pri-124-1) during erythropoiesis. QKI5 recognizes a distal QKI response element and recruits Microprocessor through interaction with DGCR8.

QKI5-mediated alternative splicing of the histone variant macroH2A1 regulates gastric carcinogenesis.

Alternative pre-mRNA splicing is a key mechanism for increasing proteomic diversity and modulating gene expression. Emerging evidence indicated that the splicing program is frequently dysregulated during tumorigenesis. Cancer cells produce protein isoforms that can promote growth and survival.