FAM32A

Last update 08 May 2025

Basic Info

Synonyms

DKFZP586O0120, FAM32A, family with sequence similarity 32 member A

+ [4]

Introduction

Isoform 1, but not isoform 2 or isoform 3, may induce G2 arrest and apoptosis. May also increase cell sensitivity to apoptotic stimuli.

100 Clinical Results associated with FAM32A

100 Translational Medicine associated with FAM32A

0 Patents (Medical) associated with FAM32A

Literatures (Medical) associated with FAM32A

01 Jan 2025·Cancer Genomics - Proteomics

FAM32ASuppression Decreases 5-Fluorouracil-induced Apoptosis and Is Associated With Poor Prognosis in Gastric Cancer

Article

Author: Kanda, Mitsuro ; Shimizu, Dai ; Umeda, Shinichi ; Hattori, Norifumi ; Nakayama, Goro ; Agatsuma, Yuya ; Tanaka, Haruyoshi ; Fujiwara, Michitaka ; Tanaka, Chie ; Hayashi, Masamichi ; Kodera, Yasuhiro

BACKGROUND/AIMThe development of new biomarkers to predict cancer patient prognosis is expected to aid in treatment selection, contributing to improved outcomes. In this study, we extracted a candidate gene associated with patient prognosis from a public database and investigated the molecular and biological functions and clinical significance of the gene in gastric cancer.MATERIALS AND METHODSWe analyzed The Cancer Genome Atlas database and identified the family with sequence similarity 32 member a (FAM32A) as a candidate gene. We investigated the clinicopathological significance of FAM32A mRNA and protein expression in 300 and 176 gastric cancer patients respectively. We evaluated the molecular and biological functions by suppressing FAM32A expression in gastric cancer cell lines using small interfering RNA.RESULTSIn the polymerase chain reaction (PCR) cohort, low FAM32A expression group showed significantly shorter disease-specific survival (DSS) [hazard ratio (HR)=1.586; 95% confidence interval (95% CI)=1.056-2.382, p=0.026]. In the immunohistochemistry cohort, the FAM32A(-) group had significantly shorter overall survival (HR=1.703; 95% CI=1.050-2.764, p=0.031) and DSS (HR=2.123; 95% CI=1.185-3.804, p=0.011). Multivariate Cox hazard analysis revealed that FAM32A(-) was an independent adverse prognostic factor for DSS (p<0.001). AGS cell lines with FAM32A knockdown exhibited significant resistance to 5-fluorouracil (5-FU) and reduced apoptosis upon 5-FU administration. Gene set enrichment analysis indicated decreased gene expression related to the p53 signaling pathway in AGS cells with FAM32A knockdown that were treated with 5-FU.CONCLUSIONFAM32A suppression decreases 5-FU-induced apoptosis. Low FAM32A expression is associated with a poor prognosis in gastric cancer, suggesting its potential as a biomarker.

01 Aug 2022·Molecular Cell

Mechanism of exon ligation by human spliceosome

Article

Author: Zhang, Xiaofeng ; Yan, Chuangye ; Zhan, Xiechao ; Lu, Yichen ; Shi, Yigong

Pre-mRNA splicing involves two sequential reactions: branching and exon ligation. The C complex after branching undergoes remodeling to become the C^∗ complex, which executes exon ligation. Here, we report cryo-EM structures of two intermediate human spliceosomal complexes, pre-C^∗-I and pre-C^∗-II, both at 3.6 Å. In both structures, the 3' splice site is already docked into the active site, the ensuing 3' exon sequences are anchored on PRP8, and the step II factor FAM192A contacts the duplex between U2 snRNA and the branch site. In the transition of pre-C^∗-I to pre-C^∗-II, the step II factors Cactin, FAM32A, PRKRIP1, and SLU7 are recruited. Notably, the RNA helicase PRP22 is positioned quite differently in the pre-C^∗-I, pre-C^∗-II, and C^∗ complexes, suggesting a role in 3' exon binding and proofreading. Together with information on human C and C^∗ complexes, our studies recapitulate a molecular choreography of the C-to-C^∗ transition, revealing mechanistic insights into exon ligation.

01 Apr 2021·Journal of Psychiatric ResearchQ2 · MEDICINE

Genome-wide DNA methylation analysis of cognitive function in middle and old-aged Chinese monozygotic twins

Q2 · MEDICINE

Article

Author: Li, Weilong ; Zhang, Dongfeng ; Wang, Weijing ; Jiang, Wenjie ; Lin, Haijun ; Wu, Yili ; Wen, Yanhua ; Li, Shuxia ; Tan, Qihua ; Xu, Chunsheng ; Tian, Xiaocao

Cognitive ability plays an important role in mental and physical well-beings in the increasingly ageing populations. Here, based on a sample of 30 cognitive function-discordant monozygotic twin pairs, we aimed to detect specific epigenetic variants potentially related to cognitive function by conducting an epigenome-wide association study (EWAS). Association between methylation level of single CpG site with cognitive function score was tested by linear mixed effect model. Functions of cis-regulatory regions and ontology enrichments were predicted by Genomic Regions Enrichment of Annotations Tool (GREAT). Differentially methylated regions (DMRs) were detected by comb-p python library. A list of 28 CpG sites were identified to reach the level of P < 1 × 10^-4, and the strongest association (cor = 0.138, P = 2.549 × 10^-6) was detected for DNA CpG site (Chr17: 40,700,490 bp) located at HSD17B1P1. The identified 14,065 genomic CpG sites (P < 0.05) were mapped to 2646 genes, especially HSD17B1P1, CUL4A, INTS8, GFI1B, ZNF467, CDH15, and PSMA1. GREAT ontology enrichments mainly highlighted nicotine pharmacodynamics pathway, GABA-B receptor II/nicotinic acetylcholine receptor/hedgehog/endothelin/Wnt signaling pathways, Parkinson disease, Huntington disease, glycolysis, neuronal system, and toll-like receptor binding. We detected 15 DMRs located at/near 16 genes, especially LINC01551, LINC02282, and FAM32A. And 32 cognitive function-associated differentially methylated genes could be replicated, such as SHANK2, ABCA2, PRDM16, NCOR2, and INPP5A. Our EWAS in monozygotic twins identify specific epigenetic variations which are significantly involved in functional genes, biological function and pathways that mediate cognitive function. The findings provide clues to further identify new diagnostic biomarkers and therapeutic targets for cognitive dysfunction.

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FAM32A

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