ACTL6A expression promotes invasion, metastasis and epithelial mesenchymal transition of colon cancer

Zeng, Zhijun; Yang, Hao; Xiao, Shuai

doi:10.1186/s12885-018-4931-3

Cited by 35 publications

(46 citation statements)

References 22 publications

(37 reference statements)

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“…Multiple actin related proteins including ARPC1B [60], ARPC5 [61], ACTL6A [62], and CFL1 [63], which are markers for aggressive cancers, were part of the up-regulated network nodes. Moreover, the upregulated genes contained proteins related to the cell cycle like BANF1 and proteins interacting with the centrosome including LAMTOR1 and RAB7A that had already been associated with PCa [64].…”

Section: Effects Of Distinct Cnas Converge On Common Proteinsmentioning

confidence: 99%

Convergent network effects along the axis of gene expression during prostate cancer progression

Charmpi

Guo

Zhong

et al. 2020

Preprint

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36Tumor-specific genomic aberrations are routinely determined by high throughput genomic 37 measurements. However, it is unclear how complex genome alterations affect molecular networks 38 through changing protein levels, and consequently biochemical states of tumor tissues. Here, we 39 investigated how tumor heterogeneity evolves during prostate cancer progression. In this study, we 40 performed proteogenomic analyses of 105 prostate samples, consisting of both benign prostatic 41 hyperplasia regions and malignant tumors, from 39 prostate cancer (PCa) patients. Exome sequencing, 42 copy number analysis, RNA sequencing and quantitative proteomic data were integrated using a network-43 based approach and related to clinical and histopathological features. In general, the number and 44 magnitude of alterations (DNA, RNA and protein) correlated with histopathological tumor grades. 45Although common sets of proteins were affected in high-grade tumors, the extent to which these proteins 46 changed their concentrations varied considerably across tumors. Our multi-layer network integration 47 identified a sub-network consisting of nine genes whose activity positively correlated with increasingly 48 aggressive tumor phenotypes. Importantly, although the effects on individual gene members were barely 49 detectable, together the perturbation of this sub-network was predictive for recurrence-free survival time. 50The multi-omics profiling of multiple tumor sites from the same patients revealed cases of likely shared 51 clonal origins as well as the occasional co-existence of multiple clonally independent tumors in the same 52 prostate. Overall, this study revealed molecular networks with remarkably convergent alterations across 53 tumor sites and patients, but it also exposed a diversity of network effects: we could not identify a single 54 sub-network that was perturbed in all high-grade tumor regions. 55 56 57

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Section: Effects Of Distinct Cnas Converge On Common Proteinsmentioning

confidence: 99%

Convergent network effects along the axis of gene expression during prostate cancer progression

Charmpi

Guo

Zhong

et al. 2020

Preprint

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“…Previous studies have shown that the expression of Arp4 changes during cell differentiation, and that depletion of Arp4 affects the progression of cell differentiation [42][43][44]. Furthermore, human Arp4 (ACTL6A) is overexpressed in various types of cancer cells, and regulates tumor growth and progression [45][46][47][48]. However, the biologic roles of Arp4 in carcinogenesis remain unknown.…”

Section: Arp4 Is Involved In Genome Functions As a Novel Suppressor Omentioning

confidence: 99%

The Actin-Family Protein Arp4 Is a Novel Suppressor for the Formation and Functions of Nuclear F-Actin

Yamazaki

Gerhold

Yamamoto

et al. 2020

Cells

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The crosstalk between actin and actin-related proteins (Arps), namely Arp2 and Arp3, plays a central role in facilitating actin polymerization in the cytoplasm and also in the nucleus. Nuclear F-actin is required for transcriptional regulation, double-strand break repair, and nuclear organization. The formation of nuclear F-actin is highly dynamic, suggesting the involvement of positive and negative regulators for nuclear actin polymerization. While actin assembly factors for nuclear F-actin have been recently described, information about inhibitory factors is still limited. The actin-related protein Arp4 which is predominantly localized in the nucleus, has been previously identified as an integral subunit of multiple chromatin modulation complexes, where it forms a heterodimer with monomeric actin. Therefore, we tested whether Arp4 functions as a suppressor of nuclear F-actin formation. The knockdown of Arp4 (Arp4 KD) led to an increase in nuclear F-actin formation in NIH3T3 cells, and purified Arp4 potently inhibited F-actin formation in mouse nuclei transplanted into Xenopus laevis oocytes. Consistently, Arp4 KD facilitated F-actin-inducible gene expression (e.g., OCT4) and DNA damage repair. Our results suggest that Arp4 has a critical role in the formation and functions of nuclear F-actin.

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“…Amplifications of ACTL6A are associated with PDAC (Table 1); however, mechanistic studies in PDAC are missing. Several studies demonstrated that ACTL6A is amplified and upregulated in different cancers [137,[281][282][283][284][285]. ACTL6A has a protumorigenic function and its expression level correlated with worse clinicopathological features in liver cancer and in colon cancer [283,284].…”

Section: Actl6amentioning

confidence: 99%

“…Several studies demonstrated that ACTL6A is amplified and upregulated in different cancers [137,[281][282][283][284][285]. ACTL6A has a protumorigenic function and its expression level correlated with worse clinicopathological features in liver cancer and in colon cancer [283,284]. Mechanistically, ACTL6A overexpression promoted migration and invasion and induced EMT in vitro [283,284] and promoted tumor growth and metastasis in a mouse liver cancer xenograft model [283].…”

Section: Actl6amentioning

confidence: 99%

“…ACTL6A has a protumorigenic function and its expression level correlated with worse clinicopathological features in liver cancer and in colon cancer [283,284]. Mechanistically, ACTL6A overexpression promoted migration and invasion and induced EMT in vitro [283,284] and promoted tumor growth and metastasis in a mouse liver cancer xenograft model [283]. Further studies demonstrated that ACTL6A targets SOX2 expression, which activates Notch1 signaling, leading to EMT [282,283].…”

Section: Actl6amentioning

confidence: 99%

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The Emerging Roles of ATP-Dependent Chromatin Remodeling Complexes in Pancreatic Cancer

Hasan

Ahuja

2019

Cancers

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Pancreatic cancer is an aggressive cancer with low survival rates. Genetic and epigenetic dysregulation has been associated with the initiation and progression of pancreatic tumors. Multiple studies have pointed to the involvement of aberrant chromatin modifications in driving tumor behavior. ATP-dependent chromatin remodeling complexes regulate chromatin structure and have critical roles in stem cell maintenance, development, and cancer. Frequent mutations and chromosomal aberrations in the genes associated with subunits of the ATP-dependent chromatin remodeling complexes have been detected in different cancer types. In this review, we summarize the current literature on the genomic alterations and mechanistic studies of the ATP-dependent chromatin remodeling complexes in pancreatic cancer. Our review is focused on the four main subfamilies: SWItch/sucrose non-fermentable (SWI/SNF), imitation SWI (ISWI), chromodomain-helicase DNA-binding protein (CHD), and INOsitol-requiring mutant 80 (INO80). Finally, we discuss potential novel treatment options that use small molecules to target these complexes.

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ACTL6A expression promotes invasion, metastasis and epithelial mesenchymal transition of colon cancer

Cited by 35 publications

References 22 publications

Convergent network effects along the axis of gene expression during prostate cancer progression

Convergent network effects along the axis of gene expression during prostate cancer progression

The Actin-Family Protein Arp4 Is a Novel Suppressor for the Formation and Functions of Nuclear F-Actin

The Emerging Roles of ATP-Dependent Chromatin Remodeling Complexes in Pancreatic Cancer

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