Leucine Zipper Down-regulated in Cancer-1 (LDOC1) interacts with Guanine nucleotide binding protein-like 3-like (GNL3L) to modulate Nuclear Factor-kappa B (NF-κB) signaling during cell proliferation

Thoompumkal, Indu Jose; Krishnan, R.; Kumaraswamy, Anbarasu; Mahalingam, Sundarasamy

doi:10.1080/15384101.2016.1242534

Cited by 27 publications

(32 citation statements)

References 53 publications

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“…Further study suggested chrysophanol could inhibit NF-κB activity. NF-κB activation has been found in many human cancers, which plays important roles in cancer proliferation, invasion and metastasis and associates with poor survival rate ( 19 – 21 ). cyclin D1 and cyclin E play pivotal roles in cell growth of many malignant cancers ( 22 , 23 ).…”

Section: Discussionmentioning

confidence: 99%

Chrysophanol inhibits proliferation and induces apoptosis through NF-κB/cyclin D1 and NF-κB/Bcl-2 signaling cascade in breast cancer cell lines

Ren

Dai

et al. 2018

Mol Med Report

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Chrysophanol is an anthraquinone compound, which exhibits anticancer effects on certain types of cancer cells. However, the effects of chrysophanol on human breast cancer remain to be elucidated. The aim of the present study was to clarify the role of chrysophanol on breast cancer cell lines MCF-7 and MDA-MB-231, and to identify the signal transduction pathways regulated by chrysophanol. MTT assay and flow cytometric analysis demonstrated that chrysophanol inhibited cell proliferation, and cell cycle progression in a dose-dependent manner. The expression of cell cycle-associated cyclin D1 and cyclin E were downregulated while p27 expression was upregulated following chrysophanol treatment at the mRNA, and protein levels. The Annexin V/propidium iodide staining assay results revealed that apoptosis levels increased following chrysophanol treatment. Chrysophanol upregulated caspase 3 and poly (ADP-ribose) polymerase cleavage in both cell lines. Furthermore, chrysophanol enhanced the effect of paclitaxel on breast cancer cell apoptosis. In addition, chrysophanol downregulated apoptosis regulator Bcl-2 protein, and transcription factor p65 and IκB phosphorylation. Inhbition of nuclear factor (NF)-κB by ammonium pyrrolidine dithiocarbamate diminished the effect of chrysophanol on apoptosis and associated proteins. In conclusion, the results of the current study demonstrated that chrysophanol effectively suppresses breast cancer cell proliferation and facilitates chemosentivity through modulation of the NF-κB signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Chrysophanol inhibits proliferation and induces apoptosis through NF-κB/cyclin D1 and NF-κB/Bcl-2 signaling cascade in breast cancer cell lines

Ren

Dai

et al. 2018

Mol Med Report

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“…The TRF1-stabilizing function of GNL3L causes a mitotic increase in TRF1, and promotes the transition from metaphase to anaphase during mitosis. GNL3L has also been suggested to participate in maintaining the function of so called tumor initiating cells [31], and in the regulation of cell proliferation during tumorigenesis by modulation of NF-κB signaling [32]. RASSF9 is associated with endosomes and is linked to vesicle trafficking [33].…”

Section: Discussionmentioning

confidence: 99%

Candidate susceptibility variants in angioimmunoblastic T-cell lymphoma

et al. 2018

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Angioimmunoblastic T-cell lymphoma (AITL) is a subtype of peripheral T-cell lymphoma with a poor prognosis: the 5-year survival rate is approximately 30%. Somatic driver mutations have been found in TET2, IDH2, DNMT3A, RHOA, FYN, PLCG1, and CD28, whereas germline susceptibility to AITL has to our knowledge not been studied. The homogenous Finnish population is well suited for studies on genetic predisposition. Here, we performed an exome-wide rare variant analysis in 23 AITL patients. No germline mutations were found in the driver genes, implying that they are not frequently involved in genetic AITL predisposition. Potentially pathogenic variants present in at least two patients and showing significant (p < 0.01) enrichment in our sample set were found in ten genes: POLK, PRKCB, ZNF676, PRRC2B, PCDHGB6, GNL3L, TTC36, OTOG, OSGEPL1, and RASSF9. The most significantly enriched variants, causing p.Lys469Ter in a splice variant of POLK and p.Pro588His in PRKCB, are intriguing candidates as Polk deficient mice display a spontaneous mutator phenotype, whereas PRKCB was recently shown to be somatically mutated in 33% of another peripheral T-cell lymphoma, adult T-cell lymphoma. If validated, our findings would provide new insight into the pathogenesis of AITL, as well as tools for early detection in susceptible individuals.

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“…HCT116 p53 +/+ or AGS cells were transfected with GNL1 1–607 , GNL1 1–607_R22K23A , RPS20-FLAG, GNL1 shRNA, RPS20 shRNA alone or in combination. MTT assay was perfomed as described previously 57 .…”

Section: Methodsmentioning

confidence: 99%

“…Total RNA from HCT116 p53 +/+ cells transfected with different expression plasmids was isolated using TRIzol reagent (TaKaRa, Japan). qPCR analysis was performed as described previously 57 . The expression levels of various genes relative to beta-actin were analyzed according to the manufacturer’s directions.…”

Section: Methodsmentioning

confidence: 99%

Interplay between human nucleolar GNL1 and RPS20 is critical to modulate cell proliferation

Krishnan

Boddapati

Mahalingam

2018

Sci Rep

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Human Guanine nucleotide binding protein like 1 (GNL1) belongs to HSR1_MMR1 subfamily of nucleolar GTPases. Here, we report for the first time that GNL1 promotes cell cycle and proliferation by inducing hyperphosphorylation of retinoblastoma protein. Using yeast two-hybrid screening, Ribosomal protein S20 (RPS20) was identified as a functional interacting partner of GNL1. Results from GST pull-down and co-immunoprecipitation assays confirmed that interaction between GNL1 and RPS20 was specific. Further, GNL1 induced cell proliferation was altered upon knockdown of RPS20 suggesting its critical role in GNL1 function. Interestingly, cell proliferation was significantly impaired upon expression of RPS20 interaction deficient GNL1 mutant suggest that GNL1 interaction with RPS20 is critical for cell growth. Finally, the inverse correlation of GNL1 and RPS20 expression in primary colon and gastric cancers with patient survival strengthen their critical importance during tumorigenesis. Collectively, our data provided evidence that cross-talk between GNL1 and RPS20 is critical to promote cell proliferation.

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Leucine Zipper Down-regulated in Cancer-1 (LDOC1) interacts with Guanine nucleotide binding protein-like 3-like (GNL3L) to modulate Nuclear Factor-kappa B (NF-κB) signaling during cell proliferation

Cited by 27 publications

References 53 publications

Chrysophanol inhibits proliferation and induces apoptosis through NF-κB/cyclin D1 and NF-κB/Bcl-2 signaling cascade in breast cancer cell lines

Chrysophanol inhibits proliferation and induces apoptosis through NF-κB/cyclin D1 and NF-κB/Bcl-2 signaling cascade in breast cancer cell lines

Candidate susceptibility variants in angioimmunoblastic T-cell lymphoma

Interplay between human nucleolar GNL1 and RPS20 is critical to modulate cell proliferation

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