Editorial Comment on “High phospho‐histone H3 expression uniquely predicts favorable survival among four markers of cellular proliferation in colorectal cancer”

2021 ◽  
Author(s):  
Hiroshi Kijima
Keyword(s):  
Colorectal Cancer ◽  
Editorial Comment ◽  
Cellular Proliferation ◽  
Histone H3

High phospho‐histone H3 expression uniquely predicts favorable survival among four markers of cellular proliferation in colorectal cancer

2021 ◽  
Author(s):  
Akira Koshino ◽  
Satoshi Inoue ◽  
Akane Sugimura‐Nagata ◽  
Takeshi Nishiyama ◽  
Hideki Murakami ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cellular Proliferation ◽  
Histone H3

scholarly journals lncRNA NORAD Contributes to Colorectal Cancer Progression by Inhibition of miR-202-5p

2018 ◽  
Vol 26 (9) ◽  
pp. 1411-1418 ◽  
Author(s):  
Jie Zhang ◽  
Xiao-Yan Li ◽  
Ping Hu ◽  
Yuan-Sheng Ding
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Noncoding Rna ◽  
Cancer Metastasis ◽  
Cellular Proliferation ◽  
Inhibitory Effect ◽  
Migration And Invasion ◽  
Competing Endogenous Rna

Previous study indicates that long noncoding RNA NORAD could serve as a competing endogenous RNA to pancreatic cancer metastasis. However, its role in colorectal cancer (CRC) needs to be investigated. In the present study, we found that the expression of NORAD was significantly upregulated in CRC tissues. Furthermore, the expression of NORAD was positively related with CRC metastasis and patients’ poor prognosis. Knockdown of NORAD markedly inhibited CRC cell proliferation, migration, and invasion but induced cell apoptosis in vitro. In vivo experiments also indicated an inhibitory effect of NORAD on tumor growth. Mechanistically, we found that NORAD served as a competing endogenous RNA for miR-202-5p. We found that there was an inverse relationship between the expression of NORAD and miR-202-5p in CRC tissues. Moreover, overexpression of miR-202-5p in SW480 and HCT116 cells significantly inhibited cellular proliferation, migration, and invasion. Taken together, our study demonstrated that the NORAD/miR-202-5p axis plays a pivotal function on CRC progression.

Abstract 115: Nuclear CaMKII is a Histone H3 Kinase that Remodels Chromatin During Cardiac Hypertrophy

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Salma Mahmoud ◽  
Muhammad Kunhi ◽  
Gillian H Little ◽  
Yan Bai ◽  
Woojin An ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Cardiac Muscle ◽  
Chromatin Remodeling ◽  
Cellular Proliferation ◽  
Recombinant Adenovirus ◽  
Phosphorylation Site ◽  
Histone H3 ◽  
Functional Link

Background and Purpose: Calcium/calmodulin-dependent protein kinase II (CaMKII) is a ubiquitous serine/threonine kinase implicated in pathological events such as cardiac hypertrophy. In this study we investigated the role of a specific nuclear isoform of CaMKII in chromatin remodeling and in transcriptional regulation in cardiac muscle. Methods: Comprehensive experimental approaches performed in primary cardiomyocyte cultures were used including chromatin immunoprecipitation assays (ChIP), q-PCR, chromatin remodeling assays, in vitro phosphorylation/transcription assays, production of recombinant adenovirus, siRNA technology, fluorescence microscopy and mass spectrometry. Results: We found that CaMKIIδB targets specific components of chromatin during cardiac hypertrophy and binds to nucleosomes through its association domain in a cooperative model. CaMKIIδB also increased chromatin relaxation, and this action was dependent on its kinase activity. The observation that CaMKIIδB interacts with chromatin suggested to us that histones maybe novel substrates of the kinase in cardiac muscle. To test this hypothesis, we performed in vitro kinase assays and found that histone H3 is a bona fide CaMKIIδB substrate and Ser-10 appears to be a predominant phosphorylation site. Increased histone H3 Ser-10 phosphorylation was observed following hypertrophic stimulation and was not associated with cellular proliferation, whereas depletion of CaMKIIδB significantly reduced histone H3 Ser-10 phosphorylation in primary cardiomyocytes. Interestingly, we found that H3 S10 phosphorylation and recruitment of CaMKIIδB occur at promoters of fetal cardiac genes. To establish the functional link between H3 phosphorylation by CaMKIIδB, chromatin remodeling and transcription activation, we developed an in vitro transcription system and using it we found that CaMKIIδB increased chromatin accessibility and mediated transcription of the Mef2 transcription factor. Conclusion: Taken together, these findings highlight a new role of CaMKIIδB as relevant histone H3 kinase and link for the first time epigenetic changes by CaMKII to cardiac hypertrophy.

scholarly journals Flavonoids and Colorectal Cancer Prevention

Antioxidants ◽  
2018 ◽  
Vol 7 (12) ◽  
pp. 187 ◽  
Author(s):  
Yanyan Li ◽  
Tao Zhang ◽  
Grace Chen
Keyword(s):  
Colorectal Cancer ◽  
Fruits And Vegetables ◽  
Cellular Proliferation ◽  
Vegetable Consumption ◽  
Inverse Association ◽  
Protective Effects ◽  
Colon Tumorigenesis ◽  
Common Cancer ◽  
Colorectal Cancer Prevention ◽  
Related Mortality

Colorectal cancer (CRC) is the third most common cancer, but despite advances in treatment, it remains the second most common cause of cancer-related mortality. Prevention may, therefore, be a key strategy in reducing colorectal cancer deaths. Given reports of an inverse association between fruit and vegetable consumption with colorectal cancer risk, there has been significant interest in understanding the metabolism and bioactivity of flavonoids, which are highly abundant in fruits and vegetables and account for their pigmentation. In this review, we discuss host and microbiota-mediated metabolism of flavonoids and the potential mechanisms by which flavonoids can exert protective effects against colon tumorigenesis, including regulation of signaling pathways involved in apoptosis, cellular proliferation, and inflammation and modulation of the gut microbiome.

Baseline Nucleophosmin Status in Mutated(M) Versus Unmutated (U) Immunoglobulin B-CLL Is a Nuclear Reflection of Different Signal Transduction Physiology.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 5005-5005
Author(s):  
Jerina Boelens ◽  
Wim Van den Berghe ◽  
Guy Haegeman ◽  
Ann Janssens ◽  
Jan Philippe ◽  
...  
Keyword(s):  
Cellular Proliferation ◽  
Histone H3 ◽  
Routine Practice ◽  
Histone H4 ◽  
Total Histone ◽  
Environmental Signals ◽  
Erk Activation ◽  
Erk Phosphorylation ◽  
The Difference

Abstract Aim: The difference in prognosis between B-CLL patients with (M) and wihout (U) somatic hypermutations of the immunoglobulin genes has led to a search for surrogate markers in routine practice. cDNA-Microarray differentiation between M and U led to further analysis of Zap-70, fibromodulin and LPLase, all of which succesfully discriminate the majority of M vs U.. In 1 of 2 proteomic studies searching the difference between M and U B-CLL, nucleophosmin came out as uniformly absent in 6 U patients and present in all 6 with M B-CLL. Nucleophosmin is a nucleolar non-ribosomal protein, associated with cellular proliferation. It is implicated in carcinogenesis as a differentiation blocker in K562 myeloid leukemias where its degradation from a 35 to a 21 kD form accompanies phorbol ester induced differentiation. In K562 this degradation is dependent on P-Erk-translocation to the nucleus that by itself depends on prolonged Erk-activation. We have recently demonstrated that SDF-1, an important microenvironment factor in B-CLL, is capable of inducing prolonged Erk-activation in Zap-70+ but not in Zap-70- B-CLL cells in vitro. This prompted us to study the unstimulated expression of nucleophosmin and other nuclear proteins by Westen blot in 16 patients with B-CLL. Methods: Histones and other alkalic proteins were extracted from the nuclei (pellet fraction) upon treatment with 0.4 M HCl. Following precipitation in acetone, histones and proteins were resuspended in sample buffer and separated by SDS PAGE or acid urea gel electrophoresis. Subsequently, the proteins were electrotransferred to a nitrocellulose membrane. Western blot analysis was performed against nucleophosmin, histone H3 or H4, and final signal detection was revealed by enhanced chemiluminescence reaction. Results: The 35 kD nucleophosmin signal was uniformly expressed in all samples and related to total histone content, irrespective of mutation status, cytogenetics and stage of disease. However, a minor band at 21 kD reflecting degradation was present in 6/6 patients with U B-CLL and absent in 8/10 with M B-CLL. Pan-histone H3 and H4 antibodies revealed similar banding patterns for histone H3 in all patients, but the presence of a heavier (probably ubiquinated) double band for histone H4 in some. This ubiquinated fraction was important in 7/16, faint in 5/16 and absent in 4/16. Morphology was atypical in 4/7 with an important fraction, and typical in all others. 5/7 with important bands and 4/5 with faint bands were M B-CLL against only 1 out of 4 in the group with absence of ubiquitination bands. Discussion: In contrast to previous proteomic studies, we found the 35 kD form of nucleophosmin present in both M and U B-CLL. However, nucleophosmin metabolisation to the 21 kD form is observed preferentially in the U B-CLL. The increased baseline degradation of nucleophosmin in 6/6 U B-CLL all of whom are Zap-70+ can be explained as a downstream nuclear signal from constitutive increased Erk-phosphorylation upon environmental signals in Zap-70+ B-CLL.

Global histone modification of histone H3 in colorectal cancer and its precursor lesions

2012 ◽  
Vol 43 (6) ◽  
pp. 834-842 ◽  
Author(s):  
Tadao Nakazawa ◽  
Tetsuo Kondo ◽  
Defu Ma ◽  
Dongfeng Niu ◽  
Kunio Mochizuki ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Histone Modification ◽  
Histone H3 ◽  
Precursor Lesions

Metformin Inhibits Cellular Proliferation and Bioenergetics in Colorectal Cancer Patient–Derived Xenografts

2017 ◽  
Vol 16 (9) ◽  
pp. 2035-2044 ◽  
Author(s):  
Nur-Afidah Mohamed Suhaimi ◽  
Wai Min Phyo ◽  
Hao Yun Yap ◽  
Sharon Heng Yee Choy ◽  
Xiaona Wei ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Patient ◽  
Cellular Proliferation ◽  
Colorectal Cancer Patient
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