Identifying LRRC16B as an oncofetal gene with transforming enhancing capability using a combined bioinformatics and experimental approach

Hsu, Che-Chia; Chiang, Chi-Wu; Cheng, Hongye; Chang, Wei-Tse; Chou, Cheng Yang; Tsai, Hung Wen; Lee, C. T.; Wu, Z. H.; Lee, T. Y.; Chao, An‐Shine; Chow, Nan Haw; Ho, Chung Liang

doi:10.1038/onc.2010.451

Cited by 19 publications

(26 citation statements)

References 46 publications

(48 reference statements)

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“…The primary amino acid sequence of CARMIL3 is more similar to that of CARMIL1 than CARMIL2. One study found that LRRC16B (the human gene encoding CARMIL3) is an oncofetal gene, whose overexpression leads to increased proliferation and tumorigenicity of transformed cells 78 .…”

Section: Allosteric Inhibition By Carmil Proteinsmentioning

confidence: 99%

Capping protein regulators fine-tune actin assembly dynamics

Edwards

Zwolak

Schafer

et al. 2014

Nat Rev Mol Cell Biol

255

269

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Capping protein (CP) regulates actin polymerization by binding the barbed end of an actin filament, which blocks addition and loss of actin subunits. Recent structural and biochemical studies provide new insight into how cells control the actin capping activity of CP. Several molecules indirectly regulate CP by interacting with filament barbed ends and preventing binding of CP; others bind directly to CP and sterically block its interaction with an actin filament. A diverse and otherwise unrelated set of proteins contains a motif for CP regulation termed the “Capping Protein Interaction” (CPI) motif. These proteins bind directly to CP, recruit or target CP to a subcellular location, and modulate its actin-capping activity via allosteric effects.

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Section: Allosteric Inhibition By Carmil Proteinsmentioning

confidence: 99%

Capping protein regulators fine-tune actin assembly dynamics

Edwards

Zwolak

Schafer

et al. 2014

Nat Rev Mol Cell Biol

255

269

View full text Add to dashboard Cite

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“…In a study of human tissues, CARMIL2 expression, assayed by reverse transcription PCR (RT-PCR), was detected in 30 different tissues, including skin (Matsuzaka et al , 2004). A study of CARMIL3 expression in human cells identified it as an oncofetal gene; it was found in brain, colon, heart, kidney, liver, lung, skeletal muscle, and spinal cord of both adult and fetal tissue samples, based on RT-PCR assays (Hsu et al , 2011). …”

Section: Roles Of Carmils At the Cellular And Organismal Levelsmentioning

confidence: 99%

CARMIL family proteins as multidomain regulators of actin-based motility

Stark

Lanier

Cooper

2017

MBoC

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CARMILs are large multidomain proteins that regulate the actin-binding activity of capping protein (CP), a major capper of actin filament barbed ends in cells. CARMILs bind directly to CP and induce a conformational change that allosterically decreases but does not abolish its actin-capping activity. The CP-binding domain of CARMIL consists of the CP-interaction (CPI) and CARMIL-specific interaction (CSI) motifs, which are arranged in tandem. Many cellular functions of CARMILs require the interaction with CP; however, a more surprising result is that the cellular function of CP in cells appears to require binding to a CARMIL or another protein with a CPI motif, suggesting that CPI-motif proteins target CP and modulate its actin-capping activity. Vertebrates have three highly conserved genes and expressed isoforms of CARMIL with distinct and overlapping localizations and functions in cells. Various domains of these CARMIL isoforms interact with plasma membranes, vimentin intermediate filaments, SH3-containing class I myosins, the dual-GEF Trio, and other adaptors and signaling molecules. These biochemical properties suggest that CARMILs play a variety of membrane-associated functions related to actin assembly and signaling. CARMIL mutations and variants have been implicated in several human diseases. We focus on roles for CARMILs in signaling in addition to their function as regulators of CP and actin.

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“…While upstream transcriptional regulators of some oncofetal genes are known (198)(199)(200)(201), surprisingly little is known about epigenetic regulation of their expression. Studies examining cancer-associated reexpression of various oncofetal genes have mostly focused on DNA methylation.…”

Section: Bivalent Chromatin: Novel Regulatory Dimensionsmentioning

confidence: 99%

“…For example, the LIN28B gene is associated with neuroblastoma (195), the HMGA2 gene is expressed in aggressive ovarian cancer (196), and IGF2BP family member genes are reactivated in a number of cancers, including breast, cervical, and hepatic cancers (197). These findings indicate that a common mechanism is operative in posttranscriptional regulation of several oncofetal genes and suggest that a common mechanism may also regulate transcriptional reactivation of these genes across cancer types.While upstream transcriptional regulators of some oncofetal genes are known (198)(199)(200)(201), surprisingly little is known about epigenetic regulation of their expression. Studies examining cancer-associated reexpression of various oncofetal genes have mostly focused on DNA methylation.…”

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confidence: 99%

Bivalent Epigenetic Control of Oncofetal Gene Expression in Cancer

Zaidi

Frietze

Gordon

et al. 2017

Molecular and Cellular Biology

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Multiple mechanisms of epigenetic control that include DNA methylation, histone modification, noncoding RNAs, and mitotic gene bookmarking play pivotal roles in stringent gene regulation during lineage commitment and maintenance. Experimental evidence indicates that bivalent chromatin domains, i.e., genome regions that are marked by both H3K4me3 (activating) and H3K27me3 (repressive) histone modifications, are a key property of pluripotent stem cells. Bivalency of developmental genes during the G 1 phase of the pluripotent stem cell cycle contributes to cell fate decisions. Recently, some cancer types have been shown to exhibit partial recapitulation of bivalent chromatin modifications that are lost along with pluripotency, suggesting a mechanism by which cancer cells reacquire properties that are characteristic of undifferentiated, multipotent cells. This bivalent epigenetic control of oncofetal gene expression in cancer cells may offer novel insights into the onset and progression of cancer and may provide specific and selective options for diagnosis as well as for therapeutic intervention.KEYWORDS bivalency, cancer, epigenetic control, nuclear structure, oncofetal gene expression E pigenetic control of gene expression plays a pivotal role in physiological responsiveness and is often compromised during onset and progression of cancer. Epigenetic changes are heritable but do not involve changes in DNA sequences. Within a given cell, there are many distinct carriers of epigenetic information that are relayed to progeny upon cell division. Epigenetic mechanisms include methylation of CpG residues, modifications of nucleosomal histone proteins, regulation of gene transcription and protein translation by noncoding RNA molecules, and mitotic retention of transcription factors (1)(2)(3)(4)(5)(6)(7)(8). From an architectural perspective, epigenetic control is engaged at multiple levels of nuclear organization from sequence-specific regulatory elements to chromatin remodeling at the nucleosomal level to large-scale inter-and intrachromosomal interactions (9)(10)(11)(12)(13)(14). These epigenetic mechanisms function in a complex but coordinated manner to orchestrate cellular responses to extracellular signals.The cellular epigenetic landscape is dynamically modified by a number of posttranslational modifications of nucleosomal histones (1,3,15,16). These modifications function in concert-a phenomenon described as the histone code-to establish context-dependent chromatin landscapes that control access of transcription factors to gene regulatory regions (1,3,15,16). This review focuses on the bivalent chromatin landscape defined by addition of three methyl moieties to lysine 4 and lysine 27 residues of histone H3 (referred to as histone 3 lysine 4 me3 [H3K4me3] and H3K27me3 throughout this article). Chromatin bivalency, i.e., the presence of both activating H3K4me3 and repressive H3K27me3 modifications at gene promoters, was first ob- Address correspondence to Gary S. Stein, gary.stein@med.uvm.edu. MINIREVIEW cr...

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Identifying LRRC16B as an oncofetal gene with transforming enhancing capability using a combined bioinformatics and experimental approach

Cited by 19 publications

References 46 publications

Capping protein regulators fine-tune actin assembly dynamics

Capping protein regulators fine-tune actin assembly dynamics

CARMIL family proteins as multidomain regulators of actin-based motility

Bivalent Epigenetic Control of Oncofetal Gene Expression in Cancer

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