CRACD

Last update 08 May 2025

Basic Info

Synonyms

Cancer-related regulator of actin dynamics, capping protein inhibiting regulator of actin dynamics, Capping protein-inhibiting regulator of actin dynamics

+ [3]

Introduction

Involved in epithelial cell integrity by acting on the maintenance of the actin cytoskeleton. Positively regulates the actin polymerization, by inhibiting the interaction of actin-capping proteins with actin.

100 Clinical Results associated with CRACD

100 Translational Medicine associated with CRACD

0 Patents (Medical) associated with CRACD

Literatures (Medical) associated with CRACD

01 Jun 2024·Cell Reports

CRACD loss induces neuroendocrine cell plasticity of lung adenocarcinoma

Article

Author: Kim, Kee-Beom ; Ko, Kyung-Pil ; Park, Jae-Il ; Zhang, Jie ; Kim, Bongjun ; Zou, Gengyi ; Jung, Youn-Sang ; Park, Kwon-Sik ; Huang, Yuanjian ; Jun, Sohee ; Jang, Jinho ; Zhang, Shengzhe

Tumor cell plasticity contributes to intratumoral heterogeneity and therapy resistance. Through cell plasticity, some lung adenocarcinoma (LUAD) cells transform into neuroendocrine (NE) tumor cells. However, the mechanisms of NE cell plasticity remain unclear. CRACD (capping protein inhibiting regulator of actin dynamics), a capping protein inhibitor, is frequently inactivated in cancers. CRACD knockout (KO) is sufficient to de-repress NE-related gene expression in the pulmonary epithelium and LUAD cells. In LUAD mouse models, Cracd KO increases intratumoral heterogeneity with NE gene expression. Single-cell transcriptomic analysis showed that Cracd KO-induced NE cell plasticity is associated with cell de-differentiation and stemness-related pathway activation. The single-cell transcriptomic analysis of LUAD patient tumors recapitulates that the distinct LUAD NE cell cluster expressing NE genes is co-enriched with impaired actin remodeling. This study reveals the crucial role of CRACD in restricting NE cell plasticity that induces cell de-differentiation of LUAD.

16 Oct 2023·Cells

lncRNA Sequencing Reveals Neurodegeneration-Associated FUS Mutations Alter Transcriptional Landscape of iPS Cells That Persists in Motor Neurons.

Article

Author: Wang, Haibo ; Kodavati, Manohar ; Guo, Wenting ; Provasek, Vincent E ; Hegde, Muralidhar L ; Van Den Bosch, Ludo ; Britz, Gavin ; Boldogh, Istvan

Fused-in sarcoma (FUS) gene mutations have been implicated in amyotrophic lateral sclerosis (ALS). This study aimed to investigate the impact of FUS mutations (R521H and P525L) on the transcriptome of induced pluripotent stem cells (iPSCs) and iPSC-derived motor neurons (iMNs). Using RNA sequencing (RNA Seq), we characterized differentially expressed genes (DEGs) and differentially expressed lncRNAs (DELs) and subsequently predicted lncRNA-mRNA target pairs (TAR pairs). Our results show that FUS mutations significantly altered the expression profiles of mRNAs and lncRNAs in iPSCs. Using this large dataset, we identified and verified six key differentially regulated TAR pairs in iPSCs that were also altered in iMNs. These target transcripts included: GPR149, NR4A, LMO3, SLC15A4, ZNF404, and CRACD. These findings indicated that selected mutant FUS-induced transcriptional alterations persist from iPSCs into differentiated iMNs. Functional enrichment analyses of DEGs indicated pathways associated with neuronal development and carcinogenesis as likely altered by these FUS mutations. Furthermore, ingenuity pathway analysis (IPA) and GO network analysis of lncRNA-targeted mRNAs indicated associations between RNA metabolism, lncRNA regulation, and DNA damage repair. Our findings provide insights into potential molecular mechanisms underlying the pathophysiology of ALS-associated FUS mutations and suggest potential therapeutic targets for the treatment of ALS.

01 May 2023·Cancer medicine

Molecular genetic positioning of small intestine and papilla of Vater carcinomas including clinicopathological classification.

Article

Author: Norose, Tomoko ; Ohnami, Sumiko ; Bando, Etsuro ; Fujiya, Keiichi ; Sugiura, Teiichi ; Urakami, Kenichi ; Shiomi, Akio ; Sasaki, Keiko ; Nakayama, Goro ; Ohike, Nobuyuki ; Akiyama, Yasuto ; Sugino, Takashi ; Yamaguchi, Ken ; Imamura, Taisuke ; Kagawa, Hiroyasu ; Uesaka, Katsuhiko ; Ohshima, Keiichi ; Nakamura, Masanori ; Ashida, Ryo ; Kodera, Yasuhiro ; Nagashima, Takeshi ; Ohgi, Katsuhisa ; Okamura, Yukiyasu

BACKGROUNDSmall intestine carcinoma (SIC) cases in Japan have recently been treated with chemotherapy according to colorectal carcinoma classification, while papilla of Vater carcinoma (PVC) cases according to cholangiocarcinoma (CHC) classification. However, few research reports support the molecular genetic validity of these therapeutic choices.PATIENTS AND METHODSHere, we investigated the clinicopathological and molecular genetic factors of SIC and PVC. We used the data from the Japanese version of The Cancer Genome Atlas. Additionally, molecular genetic data on gastric adenocarcinoma (GAD), colorectal adenocarcinoma (CRAD), pancreatic ductal adenocarcinoma (PDAC), and CHC were also referred to.RESULTSThis study consisted of tumor samples from 12 patients of SIC and three patients of PVC treated from January 2014 to March 2019. Among them, six patients had pancreatic invasion. t-Distributed stochastic neighbor embedding analysis showed that the gene expression pattern of SIC was similar not only to those of GAD and CRAD, but also to that of PDAC in the pancreatic invasion patients. In addition, PVC resembled the GAD, CRAD, and PDAC, rather than the CHC. The molecular genetic characteristics of the six patients with pancreatic invasion were: one had high microsatellite instability, two had a TP53 driver mutation, and three had tumor mutation burden values <1 mutation/Mb with no driver mutation.CONCLUSIONSIn this study, the extensive gene expression profiling of organ carcinomas newly suggests that SIC or PVC may resemble GAD, CRAD, and PDAC. In addition, the data demonstrate that pancreatic invasive patients may be classified into several subtypes using molecular genetic factors.

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CRACD

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