Coiled-coil domain containing 85B suppresses the β-catenin activity in a p53-dependent manner

Iwai, Aki; Hijikata, Makoto; Hishiki, Takayuki; Isono, Osamu; Chiba, Tsutomu; Shimotohno, Kunitada

doi:10.1038/sj.onc.1210801

Cited by 20 publications

(29 citation statements)

References 22 publications

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“…Reportedly, CCDC85B suppressed the Wnt signaling pathway by inhibiting the interaction of β‐catenin with T‐cell factor 4 in the nucleus . To elucidate the mechanisms underlying CCDC85B‐induced proliferation and invasion of lung cancer cells, we investigated the Wnt signaling pathway.…”

Section: Resultssupporting

confidence: 50%

“…Du et al have found that CCDC85B interacts with p78/MCRS/MSP58 and has a role in the regulation of gene expression and cell proliferation. Furthermore, CCDC85B is also involved in Wnt signaling pathway by inhibiting the interaction of β‐catenin with the T‐cell factor 4 in the nucleus . These results indicated that CCDC85B might function in tumorigenesis and tumor progression.…”

Section: Introductionmentioning

confidence: 99%

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CCDC85B promotes non‐small cell lung cancer cell proliferation and invasion

Feng

Gao

et al. 2018

Molecular Carcinogenesis

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Coiled‐coil domain containing 85 B (CCDC85B) is involved in diverse biological processes; however, its expression patterns and functions in human cancers are yet unknown. The present study demonstrated that the expression of CCDC85B in the cytoplasm of the non‐small cell lung cancer (NSCLC) tumor cells was significantly higher compared to adjacent normal lung tissues (P < 0.05). Furthermore, CCDC85B expression correlated with advanced TNM stage (P = 0.004) and positive regional lymph node metastasis (P = 0.009) of NSCLC. In addition, in A549 and H1299 lung cancer cell lines, the overexpression of CCDC85B promoted cell proliferation and invasion, while siRNA‐mediated CCDC85B knockdown exhibited opposite effects. CCDC85B promoted AKT and GSK3β phosphorylation and upregulated the levels of active β‐catenin, Wnt targets c‐myc, cyclin D1, and MMP7. Besides, the CCDC85B‐induced upregulation of phosphorylated GSK3β and active β‐catenin was rescued following the treatment with PI3 K inhibitor, LY294002. In conclusion, CCDC85B was associated with NSCLC progression as it promoted the proliferation and invasion of lung cancer cells through activated AKT/GSK3β/β‐catenin oncogenic signaling pathway. Therefore, CCDC85B might serve as a novel target for NSCLC treatment.

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Section: Resultssupporting

confidence: 50%

Section: Introductionmentioning

confidence: 99%

CCDC85B promotes non‐small cell lung cancer cell proliferation and invasion

Feng

Gao

et al. 2018

Molecular Carcinogenesis

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“…The MAbs showed predominantly nuclear and cytoplasmic staining in most cell lines, which is consistent with previous reports. (12)(13)(14) Surprisingly some antibodies recognized DIPA at cell-cell junctions, which is unreported in the literature. MAbs 2G7 and 3E3 produced junctional staining patterns in MDCK cells.…”

Section: Immunofluorescencementioning

confidence: 90%

“…DIPA can endogenously regulate adipocyte differentiation by inhibiting C/EBP-b and C/EBP-g. (13) When induced by p53 activation, DIPA can compete with b-catenin for binding to the TCF4 transcription factor, which effectively down-regulates Wnt target gene expression. (14) Thus, DIPA is mostly found in the nucleus and appears to function primarily in transcriptional regulation.…”

Section: Introductionmentioning

confidence: 99%

“…TCF proteins can bind directly to b-catenin, DIPA, and the transcription factor Kaiso, a BTB/POZ zinc-finger protein first discovered as a p120 binding partner. (14)(15)(16) Notably, the b-catenin destruction complex, which is inhibited by Wnt stimulation and mutated in most colorectal cancer, appears to selectively ubiquitylate and degrade p120 isoform 1. (17) Thus, several lines of evidence suggest that p120 isoform 1, and by association DIPA, is functionally distinct, perhaps analogous in some respects to the cytoplasmic pool of b-catenin involved in canonical Wnt signaling.…”

Section: Introductionmentioning

confidence: 99%

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Monoclonal Antibodies to DIPA: A Novel Binding Partner of p120-Catenin Isoform 1

et al. 2012

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The coiled-coil domain-containing delta-interacting protein A (DIPA) is a transcription factor implicated in developmental regulation. DIPA is the first protein discovered to selectively interact with the p120-catenin (p120) isoform 1, an alternatively spliced form of p120 expressed preferentially in mesenchymal cells. Although a small fraction of p120 can be observed in the nucleus under certain circumstances, the vast majority of it associates with classical cadherins at adherens junctions. We observed for the first time that a discrete fraction of DIPA exists at cell-cell junctions, in addition to its predominantly nuclear localization. Thus, the p120-DIPA interaction may regulate cell signaling and/or transcriptional events, as has been described previously for b-catenin and the LEF/TCF transcription factor family. To facilitate further study of DIPA and to determine the physiological relevance of its interaction with p120, we have generated and characterized a panel of five DIPAspecific monoclonal antibodies (MAbs) that function in immunoblotting, immunoprecipitation, and immunofluorescence assays.

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Transcriptomic Profiles Associated with Experimental Placebo Effects in Chronic Pain

Colloca,

Mocci,

Wang

et al. 2024

Clin Pharma and Therapeutics

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Gene expression networks associated with placebo effects are understudied; in this study, we identified transcriptomic profiles associated with placebo responsivity. Participants suffering from chronic pain underwent a verbal suggestion and conditioning paradigm with individually tailored thermal painful stimulations to elicit conditioned placebo effects. Participants reported pain intensity on a visual analog scale (VAS) anchored from zero = no pain to 100 = maximum imaginable pain. RNA was extracted from venous blood and RNA sequencing and validation tests were performed to identify differentially expressed genes (DEGs) associated with placebo effects, controlling for sex and level of pain. Unbiased enrichment analyses were performed to identify biological processes associated with placebo effects. Of the 10,700 protein‐coding genes that passed quality control filters, 667 were found to be associated with placebo effects (FDR <0.05). Most genes (97%) upregulated were associated with larger placebo effects. The 17 top transcriptome‐wide significant genes were further validated via RT‐qPCR in an independent cohort of chronic pain participants. Six of them (CCDC85B, FBXL15, HAGH, PI3, SELENOM, and TNFRSF4) showed positive and significant (P < 0.05) correlation with placebo effects in the cohort. The overall DEGs were highly enriched in regulation of expression of SLITs and ROBOs (R‐HSA‐9010553, FDR = 1.26e−33), metabolism of RNA (R‐HSA‐8953854, FDR = 1.34e−30), Huntington's disease (hsa05016, FDR = 9.84e−31), and ribosome biogenesis (GO:0042254, FDR = 2.67e−15); alternations in these pathways might jeopardize the proneness to elicit placebo effects. Future studies are needed to replicate this finding and better understand the unique molecular dynamics of people who are more or less affected by pain and placebo.

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Coiled-coil domain containing 85B suppresses the β-catenin activity in a p53-dependent manner

Cited by 20 publications

References 22 publications

CCDC85B promotes non‐small cell lung cancer cell proliferation and invasion

CCDC85B promotes non‐small cell lung cancer cell proliferation and invasion

Monoclonal Antibodies to DIPA: A Novel Binding Partner of p120-Catenin Isoform 1

Transcriptomic Profiles Associated with Experimental Placebo Effects in Chronic Pain

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