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Article ; Online: Epigenetics Mechanisms of Honeybees: Secrets of Royal Jelly.

Alhosin, Mahmoud

Epigenetics insights

2023 Volume 16, Page(s) 25168657231213717

Abstract: Early diets in honeybees have effects on epigenome with consequences on their phenotype. Depending on the early larval diet, either royal jelly (RJ) or royal worker, 2 different female castes are generated from identical genomes, a long-lived queen with ... ...

Abstract	Early diets in honeybees have effects on epigenome with consequences on their phenotype. Depending on the early larval diet, either royal jelly (RJ) or royal worker, 2 different female castes are generated from identical genomes, a long-lived queen with fully developed ovaries and a short-lived functionally sterile worker. To generate these prominent physiological and morphological differences between queen and worker, honeybees utilize epigenetic mechanisms which are controlled by nutritional input. These mechanisms include DNA methylation and histone post-translational modifications, mainly histone acetylation. In honeybee larvae, DNA methylation and histone acetylation may be differentially altered by RJ. This diet has biologically active ingredients with inhibitory effects on the
Language	English
Publishing date	2023-11-29
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2516-8657
ISSN (online)	2516-8657
DOI	10.1177/25168657231213717
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Article ; Online: Curcumin, its derivatives, and their nanoformulations: Revolutionizing cancer treatment.

Ahmad, Iftikhar / Ahmad, Sameer / Ahmad, Ausaf / Zughaibi, Torki A / Alhosin, Mahmoud / Tabrez, Shams

Cell biochemistry and function

2024 Volume 42, Issue 1, Page(s) e3911

Abstract: Curcumin is a natural compound derived from turmeric and can target malignant tumor molecules involved in cancer propagation. It has potent antioxidant activity, but its effectiveness is limited due to poor absorption and rapid elimination from the body. ...

Abstract	Curcumin is a natural compound derived from turmeric and can target malignant tumor molecules involved in cancer propagation. It has potent antioxidant activity, but its effectiveness is limited due to poor absorption and rapid elimination from the body. Various curcumin derivatives have also shown anticancer potential in in-vitro and in-vivo models. Curcumin can target multiple signaling pathways involved in cancer development/progression or induce cancer cell death through apoptosis. In addition, curcumin and its derivatives could also enhance the effectiveness of conventional chemotherapy, radiation therapy and reduce their associated side effects. Lately, nanoparticle-based delivery systems are being developed/explored to overcome the challenges associated with curcumin's delivery, increasing its overall efficacy. The use of an imaging system to track these formulations could also give beneficial information about the bioavailability and distribution of the nano-curcumin complex. In conclusion, curcumin holds significant promise in the fight against cancer, especially in its nanoform, and could provide precise delivery to cancer cells without affecting normal healthy cells.
MeSH term(s)	Curcumin/pharmacology ; Apoptosis ; Cell Death ; Curcuma ; Nanoparticles ; Neoplasms/drug therapy
Chemical Substances	Curcumin (IT942ZTH98)
Language	English
Publishing date	2024-01-24
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	283643-9
ISSN	1099-0844 ; 0263-6484
ISSN (online)	1099-0844
ISSN	0263-6484
DOI	10.1002/cbf.3911
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Article ; Online: HAUSP Is a Key Epigenetic Regulator of the Chromatin Effector Proteins.

Abdullah, Omeima / Alhosin, Mahmoud

Genes

2021 Volume 13, Issue 1

Abstract: HAUSP (herpes virus-associated ubiquitin-specific protease), also known as Ubiquitin Specific Protease 7, plays critical roles in cellular processes, such as chromatin biology and epigenetics, through the regulation of different signaling pathways. HAUSP ...

Abstract	HAUSP (herpes virus-associated ubiquitin-specific protease), also known as Ubiquitin Specific Protease 7, plays critical roles in cellular processes, such as chromatin biology and epigenetics, through the regulation of different signaling pathways. HAUSP is a main partner of the "Epigenetic Code Replication Machinery," ECREM, a large protein complex that includes several epigenetic players, such as the ubiquitin-like containing plant homeodomain (PHD) and an interesting new gene (RING), finger domains 1 (UHRF1), as well as DNA methyltransferase 1 (DNMT1), histone deacetylase 1 (HDAC1), histone methyltransferase G9a, and histone acetyltransferase TIP60. Due to its deubiquitinase activity and its ability to team up through direct interactions with several epigenetic regulators, mainly UHRF1, DNMT1, TIP60, the histone lysine methyltransferase EZH2, and the lysine-specific histone demethylase LSD1, HAUSP positions itself at the top of the regulatory hierarchies involved in epigenetic silencing of tumor suppressor genes in cancer. This review highlights the increasing role of HAUSP as an epigenetic master regulator that governs a set of epigenetic players involved in both the maintenance of DNA methylation and histone post-translational modifications.
MeSH term(s)	Animals ; Chromatin/genetics ; Chromatin/metabolism ; DNA Methylation ; Epigenesis, Genetic ; Gene Expression Regulation ; Humans ; Ubiquitin-Specific Peptidase 7/genetics ; Ubiquitin-Specific Peptidase 7/metabolism
Chemical Substances	Chromatin ; Ubiquitin-Specific Peptidase 7 (EC 3.4.19.12)
Language	English
Publishing date	2021-12-24
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes13010042
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Article ; Online: Interlinking of diabetes mellitus and cancer: An overview.

Ahmad, Iftikhar / Suhail, Mohd / Ahmad, Ausaf / Alhosin, Mahmoud / Tabrez, Shams

Cell biochemistry and function

2023 Volume 41, Issue 5, Page(s) 506–516

Abstract: Cancer and diabetes mellitus (DM) are among the leading causes of mortality and morbidity in the global arena. Lately, several studies demonstrated that DM could promote cancer. However, the exact mechanism(s) highlighting this association are largely ... ...

Abstract	Cancer and diabetes mellitus (DM) are among the leading causes of mortality and morbidity in the global arena. Lately, several studies demonstrated that DM could promote cancer. However, the exact mechanism(s) highlighting this association are largely untouched and require comprehensive detailing. In the present review, we aimed to explore and decipher the possible mechanism of DM an cancer association. Hyperglycemia could be a subordinate plausible explanation of carcinogenesis in the diabatic patient. It is well known that high glucose levels may help in cancer proliferation. In addition, chronic inflammation, the other well-known factor of diabetes, could also play a role in carcinogenesis. Moreover, the numerous medicines to treat diabetes either increase or reduce cancer risk. Insulin is one of the potent growth factors that promotes cell propagation and induces cancer directly or via insulin like growth factor-1. On the other hand, hyperinsulinemia leads to an increased activity of growth factor-1 by inhibiting growth factor binding protein-1. To improve cancer prognosis, individuals with diabetes should be screened to discover cancer at an early stage and treated appropriately.
MeSH term(s)	Humans ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/metabolism ; Neoplasms/drug therapy ; Insulin/metabolism ; Hyperinsulinism ; Carcinogenesis ; Diabetes Mellitus/drug therapy
Chemical Substances	Insulin
Language	English
Publishing date	2023-05-18
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	283643-9
ISSN	1099-0844 ; 0263-6484
ISSN (online)	1099-0844
ISSN	0263-6484
DOI	10.1002/cbf.3802
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Article: HAUSP Is a Key Epigenetic Regulator of the Chromatin Effector Proteins

Abdullah, Omeima / Alhosin, Mahmoud

Genes. 2021 Dec. 24, v. 13, no. 1

2021

Abstract	HAUSP (herpes virus-associated ubiquitin-specific protease), also known as Ubiquitin Specific Protease 7, plays critical roles in cellular processes, such as chromatin biology and epigenetics, through the regulation of different signaling pathways. HAUSP is a main partner of the “Epigenetic Code Replication Machinery,” ECREM, a large protein complex that includes several epigenetic players, such as the ubiquitin-like containing plant homeodomain (PHD) and an interesting new gene (RING), finger domains 1 (UHRF1), as well as DNA methyltransferase 1 (DNMT1), histone deacetylase 1 (HDAC1), histone methyltransferase G9a, and histone acetyltransferase TIP60. Due to its deubiquitinase activity and its ability to team up through direct interactions with several epigenetic regulators, mainly UHRF1, DNMT1, TIP60, the histone lysine methyltransferase EZH2, and the lysine-specific histone demethylase LSD1, HAUSP positions itself at the top of the regulatory hierarchies involved in epigenetic silencing of tumor suppressor genes in cancer. This review highlights the increasing role of HAUSP as an epigenetic master regulator that governs a set of epigenetic players involved in both the maintenance of DNA methylation and histone post-translational modifications.
Keywords	DNA methylation ; DNA methyltransferase ; chromatin ; epigenetics ; histone acetyltransferase ; histone deacetylase ; histone demethylases ; histones ; lysine ; neoplasms ; proteinases ; ubiquitin
Language	English
Dates of publication	2021-1224
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes13010042
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: A Fast Ubiquitination of UHRF1 Oncogene Is a Unique Feature and a Common Mechanism of Thymoquinone in Cancer Cells

Mahmoud Alhosin / Omeima Abdullah / Asaad Kayali / Ziad Omran

Applied Sciences, Vol 11, Iss 7633, p

2021 Volume 7633

Abstract: Downregulation of the ubiquitin-like containing PHD and ring finger 1 (UHRF1) oncogene in cancer cells in response to natural anticancer drugs, including thymoquinone (TQ), is a key event that induces apoptosis. TQ can induce UHRF1 autoubiquitination via ...

Abstract	Downregulation of the ubiquitin-like containing PHD and ring finger 1 (UHRF1) oncogene in cancer cells in response to natural anticancer drugs, including thymoquinone (TQ), is a key event that induces apoptosis. TQ can induce UHRF1 autoubiquitination via the E3 ligase activity of its RING domain, most likely through the downregulation of herpes virus-associated ubiquitin-specific protease (HAUSP). In this study, we evaluated whether HAUSP downregulation and fast ubiquitination of UHRF1 are prerequisites for UHRF1 degradation in response to TQ in cancer cells and whether doxorubicin can mimic the effects of TQ on UHRF1 ubiquitination. RNA sequencing was performed to investigate differentially expressed genes in TQ-treated Jurkat cells. The protein expression of UHRF1, HAUSP and Bcl-2 was detected by means of Western blot analysis. The proliferation of human colon cancer (HCT-116) and Jurkat cells was analyzed via the WST-1 assay. RNA sequencing data revealed that TQ significantly decreased HAUSP expression. TQ triggered UHRF1 to undergo rapid ubiquitination as the first step in its degradation and the inhibition of its cell proliferation. TQ-induced UHRF1 ubiquitination is associated with HAUSP downregulation. Like TQ, doxorubicin induced a similar dose- and time-dependent downregulation of UHRF1 in cancer cells, but UHRF1 did not undergo ubiquitination as detected in response to TQ. Furthermore, TQ decreased Bcl-2 expression without triggering its ubiquitination. A fast UHRF1 ubiquitination is an indispensable event for its degradation in response to TQ but not for its responses to doxorubicin. TQ appears to trigger ubiquitination of UHRF1 but not of the Bcl-2 oncogene, thereby identifying UHRF1 as a specific target of TQ for cancer therapy.
Keywords	thymoquinone ; UHRF1 ; ubiquitination ; HAUSP ; tumor suppressor genes ; Technology ; T ; Engineering (General). Civil engineering (General) ; TA1-2040 ; Biology (General) ; QH301-705.5 ; Physics ; QC1-999 ; Chemistry ; QD1-999
Subject code	616
Language	English
Publishing date	2021-08-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: UHRF1 poly-auto-ubiquitination induced by the anti-cancer drug, thymoquinone, is involved in the DNA repair machinery recruitment.

Almalki, Naif A R / Sabir, Jamal S M / Ibrahim, Abdulkhaleg / Alhosin, Mahmoud / Asseri, Amer H / Albiheyri, Raed S / Zari, Ali T / Bahieldin, Ahmed / Javed, Aqib / Mély, Yves / Hamiche, Ali / Mousli, Marc / Bronner, Christian

The international journal of biochemistry & cell biology

2024 , Page(s) 106582

Abstract: DNA methylation is one of the most important epigenetic mark involved in many physiologic cellular processes and pathologies. During mitosis, the transmission of DNA methylation patterns from a mother to the daughter cells is ensured through the action ... ...

Abstract	DNA methylation is one of the most important epigenetic mark involved in many physiologic cellular processes and pathologies. During mitosis, the transmission of DNA methylation patterns from a mother to the daughter cells is ensured through the action of the Ubiquitin-like, containing PHD and RING domains, 1/DNA methyltransferase 1 (UHRF1/DNMT1) tandem. UHRF1 is involved in the silencing of many tumor suppressor genes (TSGs) via mechanisms that remain largely to be deciphered. The present study investigated the role and the regulation of UHRF1 poly-ubiquitination induced by thymoquinone, a natural anti-cancer drug, known to enhance or re-activate the expression of TSGs. We found that the auto-ubiquitination of UHRF1, induced by TQ, is mediated by reactive oxygen species, and occurs following DNA damage. We demonstrated that the poly-ubiquitinated form of UHRF1 is K63-linked and can still silence the tumor suppressor gene p16
Language	English
Publishing date	2024-04-20
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1228429-4
ISSN	1878-5875 ; 1357-2725
ISSN (online)	1878-5875
ISSN	1357-2725
DOI	10.1016/j.biocel.2024.106582
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Article ; Online: In Vitro and In Vivo Preventive Effects of Thymoquinone against Breast Cancer: Role of DNMT1.

Kaleem, Mohammed / Kayali, Asaad / Sheikh, Ryan A / Kuerban, Abudukadeer / Hassan, Mohammed A / Almalki, Naif Abdullah R / Al-Abbasi, Fahad A / Anwar, Firoz / Omran, Ziad / Alhosin, Mahmoud

Molecules (Basel, Switzerland)

2024 Volume 29, Issue 2

Abstract: Breast cancer (BC) is one of the most common cancers in women and is a major cause of female cancer-related deaths. BC is a multifactorial disease caused by the dysregulation of many genes, raising the need to find novel drugs that function by targeting ... ...

Abstract	Breast cancer (BC) is one of the most common cancers in women and is a major cause of female cancer-related deaths. BC is a multifactorial disease caused by the dysregulation of many genes, raising the need to find novel drugs that function by targeting several signaling pathways. The antitumoral drug thymoquinone (TQ), found in black seed oil, has multitargeting properties against several signaling pathways. This study evaluated the inhibitory effects of TQ on the MCF7 and T47D human breast cancer cell lines and its antitumor activity against BC induced by a single oral dose (65 mg/kg) of 7,12-dimethylbenzanthracene (DMBA) in female rats. The therapeutic activity was evaluated in DMBA-treated rats who received oral TQ (50 mg/kg) three times weekly. TQ-treated MCF7 and T47D cells showed concentration-dependent inhibition of cell proliferation and induction of apoptosis. TQ also decreased the expression of DNA methyltransferase 1 (DNMT1) in both cancer cell types. In DMBA-treated animals, TQ inhibited the number of liver and kidney metastases. These effects were associated with a reduction in DNMT1 mRNA expression. These results indicate that TQ has protective effects against breast carcinogens through epigenetic mechanisms involving DNMT1 inhibition.
MeSH term(s)	Female ; Humans ; Animals ; Rats ; Breast Neoplasms/chemically induced ; Breast Neoplasms/drug therapy ; Benzoquinones/pharmacology ; 9,10-Dimethyl-1,2-benzanthracene/toxicity ; Apoptosis
Chemical Substances	thymoquinone (O60IE26NUF) ; Benzoquinones ; 9,10-Dimethyl-1,2-benzanthracene (57-97-6)
Language	English
Publishing date	2024-01-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules29020434
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Article: Coordinated Dialogue between UHRF1 and DNMT1 to Ensure Faithful Inheritance of Methylated DNA Patterns.

Bronner, Christian / Alhosin, Mahmoud / Hamiche, Ali / Mousli, Marc

Genes

2019 Volume 10, Issue 1

Abstract: DNA methylation, catalyzed by DNA methyltransferases (DNMTs), is an epigenetic mark that needs to be faithfully replicated during mitosis in order to maintain cell phenotype during successive cell divisions. This epigenetic mark is located on the 5'- ... ...

Abstract	DNA methylation, catalyzed by DNA methyltransferases (DNMTs), is an epigenetic mark that needs to be faithfully replicated during mitosis in order to maintain cell phenotype during successive cell divisions. This epigenetic mark is located on the 5'-carbon of the cytosine mainly within cytosine⁻phosphate⁻guanine (CpG) dinucleotides. DNA methylation is asymmetrically positioned on both DNA strands, temporarily generating a hemi-methylated state after DNA replication. Hemi-methylation is a particular status of DNA that is recognized by ubiquitin-like containing plant homeodomain (PHD) and really interesting new gene (RING) finger domains 1 (UHRF1) through its SET- (Su(var)3-9, Enhancer-of-zeste and Trithorax) and RING-associated (SRA) domain. This interaction is considered to be involved in the recruitment of DNMT1 to chromatin in order to methylate the adequate cytosine on the newly synthetized DNA strand. The UHRF1/DNMT1 tandem plays a pivotal role in the inheritance of DNA methylation patterns, but the fine-tuning mechanism remains a mystery. Indeed, because DNMT1 experiences difficulties in finding the cytosine to be methylated, it requires the help of a guide, i.e., of UHRF1, which exhibits higher affinity for hemi-methylated DNA vs. non-methylated DNA. Two models of the UHRF1/DNMT1 dialogue were suggested to explain how DNMT1 is recruited to chromatin: (i) an indirect communication via histone H3 ubiquitination, and (ii) a direct interaction of UHRF1 with DNMT1. In the present review, these two models are discussed, and we try to show that they are compatible with each other.
MeSH term(s)	Animals ; CCAAT-Enhancer-Binding Proteins/metabolism ; DNA (Cytosine-5-)-Methyltransferase 1/metabolism ; DNA Methylation ; Epigenesis, Genetic ; Humans
Chemical Substances	CCAAT-Enhancer-Binding Proteins ; DNA (Cytosine-5-)-Methyltransferase 1 (EC 2.1.1.37) ; UHRF1 protein, human (EC 2.3.2.27)
Language	English
Publishing date	2019-01-18
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes10010065
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Article ; Online: Thymoquinone Is a Multitarget Single Epidrug That Inhibits the UHRF1 Protein Complex.

Abdullah, Omeima / Omran, Ziad / Hosawi, Salman / Hamiche, Ali / Bronner, Christian / Alhosin, Mahmoud

Genes

2021 Volume 12, Issue 5

Abstract: Silencing of tumor suppressor genes (TSGs) through epigenetic mechanisms, mainly via abnormal promoter DNA methylation, is considered a main mechanism of tumorigenesis. The abnormal DNA methylation profiles are transmitted from the cancer mother cell to ... ...

Abstract	Silencing of tumor suppressor genes (TSGs) through epigenetic mechanisms, mainly via abnormal promoter DNA methylation, is considered a main mechanism of tumorigenesis. The abnormal DNA methylation profiles are transmitted from the cancer mother cell to the daughter cells through the involvement of a macromolecular complex in which the ubiquitin-like containing plant homeodomain (PHD), and an interesting new gene (RING) finger domains 1 (UHRF1), play the role of conductor. Indeed, UHRF1 interacts with epigenetic writers, such as DNA methyltransferase 1 (DNMT1), histone methyltransferase G9a, erasers like histone deacetylase 1 (HDAC1), and functions as a hub protein. Thus, targeting UHRF1 and/or its partners is a promising strategy for epigenetic cancer therapy. The natural compound thymoquinone (TQ) exhibits anticancer activities by targeting several cellular signaling pathways, including those involving UHRF1. In this review, we highlight TQ as a potential multitarget single epidrug that functions by targeting the UHRF1/DNMT1/HDAC1/G9a complex. We also speculate on the possibility that TQ might specifically target UHRF1, with subsequent regulatory effects on other partners.
MeSH term(s)	Benzoquinones/pharmacology ; CCAAT-Enhancer-Binding Proteins/antagonists & inhibitors ; Carcinogenesis/drug effects ; Carcinogenesis/metabolism ; DNA (Cytosine-5-)-Methyltransferase 1/metabolism ; DNA Methylation/drug effects ; Epigenesis, Genetic/drug effects ; Humans ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Promoter Regions, Genetic/drug effects ; Signal Transduction/drug effects ; Ubiquitin-Protein Ligases/antagonists & inhibitors
Chemical Substances	Benzoquinones ; CCAAT-Enhancer-Binding Proteins ; DNA (Cytosine-5-)-Methyltransferase 1 (EC 2.1.1.37) ; UHRF1 protein, human (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; thymoquinone (O60IE26NUF)
Language	English
Publishing date	2021-04-22
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes12050622
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