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  1. AU="Sakuma, Ikki"
  2. AU="Cherniack, Andrew D."
  3. AU="Beitollahi, Hadi"
  4. AU="Hai-Tao Tang"
  5. AU=Rouse Benjamin AU=Rouse Benjamin
  6. AU="Rabensteiner, Toni"
  7. AU="Chowdhury, Forhad Uddin Hassan" AU="Chowdhury, Forhad Uddin Hassan"
  8. AU=Verdone Loredana AU=Verdone Loredana
  9. AU="Venegas, M"
  10. AU="Burtnick, Mary N"
  11. AU=Frisoni Giovanni B
  12. AU="Dhiraj Kumar"
  13. AU="Isaac S. Lee"
  14. AU="Bals, Julia"
  15. AU="Rovira-Clavé, Xavier"
  16. AU="Den Boer, Monique L"
  17. AU="Potts, T."
  18. AU="Cifuentes-Diaz, Carmen"
  19. AU="Alvim, Ricardo G"
  20. AU="Barron II, Joseph C"
  21. AU="Godin, Shea-Lee"
  22. AU="Leng, Chengcai"
  23. AU="Hyslop, Brian W"
  24. AU="Suzanne Fischer"
  25. AU="Aboelata, Noha"
  26. AU="Chiang, Sarah N"
  27. AU="Wessel, Kristin M"
  28. AU="Wilson, Jenna M"
  29. AU="Goines, Paula"
  30. AU=Ippolito Mariachiara AU=Ippolito Mariachiara
  31. AU="Jose Chauca"
  32. AU="Asih, Puji B S"
  33. AU="Dsane-Selby, Lydia"
  34. AU="Tolossa, Tadesse"
  35. AU="Erdal Bedir"

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  1. Artikel ; Online: Fatty Acid Esterification as a NASH Therapeutic Target.

    Sakuma, Ikki / Vatner, Daniel F

    Cellular and molecular gastroenterology and hepatology

    2023  Band 17, Heft 2, Seite(n) 311–312

    Mesh-Begriff(e) Humans ; Fatty Acids ; Esterification ; Non-alcoholic Fatty Liver Disease/drug therapy
    Chemische Substanzen Fatty Acids
    Sprache Englisch
    Erscheinungsdatum 2023-11-17
    Erscheinungsland United States
    Dokumenttyp Editorial ; Comment
    ZDB-ID 2819778-1
    ISSN 2352-345X ; 2352-345X
    ISSN (online) 2352-345X
    ISSN 2352-345X
    DOI 10.1016/j.jcmgh.2023.10.011
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: iPSCs and aging.

    Sakuma, Ikki / Tanaka, Tomoaki

    Nihon rinsho. Japanese journal of clinical medicine

    2018  Band 74, Heft 9, Seite(n) 1560–1564

    Abstract: In addition to the discovery that mature cells can be reprogrammed to become pluripotent stem cells(iPS cells), the technical innovations of big-data analyses as well as the cutting- edge technologies such as nuclear reprogramming technique and genome- ... ...

    Abstract In addition to the discovery that mature cells can be reprogrammed to become pluripotent stem cells(iPS cells), the technical innovations of big-data analyses as well as the cutting- edge technologies such as nuclear reprogramming technique and genome-editing system are emerging a big paradigm shift in the field of regenerative medicine and aging. This is bonafide a kind of the molecular biological movement of the Renaissance to answer the question of 120 years ago "D'ofi Venons Nous Que Sommes Nous Oi Allons Nous", a testament of Paul Gauguin. These technologies enable us, particularly inexhaustible researchers with challenging spirits, not only to dynamically, qualitatively and visually systematically understand underling mechanisms of single gene, single molecule, single cell and their complicated networks in vivo with broadly combining them from cells to organs and individuals', but also to pursue the mechanistic insight into "Life, Aging, Disease, and Death" and thereby con- trol them. We herein review about recent hot topic findings focused on regenerative medicine, cellular senescence & aging as well as aging-related disease, and then discuss the functional interconnection between reprogramming process and senescence signal.
    Mesh-Begriff(e) Aging/genetics ; Animals ; Cellular Reprogramming ; Cellular Senescence ; Humans ; Induced Pluripotent Stem Cells ; Regenerative Medicine
    Sprache Japanisch
    Erscheinungsdatum 2018-12-17
    Erscheinungsland Japan
    Dokumenttyp Journal Article ; Review
    ZDB-ID 390903-7
    ISSN 0047-1852
    ISSN 0047-1852
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Lysophosphatidic acid triggers inflammation in the liver and white adipose tissue in rat models of 1-acyl-sn-glycerol-3-phosphate acyltransferase 2 deficiency and overnutrition.

    Sakuma, Ikki / Gaspar, Rafael C / Luukkonen, Panu K / Kahn, Mario / Zhang, Dongyan / Zhang, Xuchen / Murray, Sue / Golla, Jaya Prakash / Vatner, Daniel F / Samuel, Varman T / Petersen, Kitt Falk / Shulman, Gerald I

    Proceedings of the National Academy of Sciences of the United States of America

    2023  Band 120, Heft 52, Seite(n) e2312666120

    Abstract: AGPAT2 (1-acyl-sn-glycerol-3-phosphate-acyltransferase-2) converts lysophosphatidic acid (LPA) into phosphatidic acid (PA), and mutations of ... ...

    Abstract AGPAT2 (1-acyl-sn-glycerol-3-phosphate-acyltransferase-2) converts lysophosphatidic acid (LPA) into phosphatidic acid (PA), and mutations of the
    Mesh-Begriff(e) Male ; Rats ; Animals ; Acyltransferases/metabolism ; Glycerol ; 1-Acylglycerol-3-Phosphate O-Acyltransferase/genetics ; 1-Acylglycerol-3-Phosphate O-Acyltransferase/metabolism ; Rats, Sprague-Dawley ; Lipodystrophy/genetics ; Fatty Liver ; Adipose Tissue, White/metabolism ; Phosphatidic Acids ; Inflammation ; Overnutrition ; Phosphates
    Chemische Substanzen Acyltransferases (EC 2.3.-) ; lysophosphatidic acid (PG6M3969SG) ; Glycerol (PDC6A3C0OX) ; 1-Acylglycerol-3-Phosphate O-Acyltransferase (EC 2.3.1.51) ; Phosphatidic Acids ; Phosphates
    Sprache Englisch
    Erscheinungsdatum 2023-12-21
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2312666120
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: O

    Nakamoto, Akiko / Ohashi, Natsuko / Sugawara, Lucia / Morino, Katsutaro / Ida, Shogo / Perry, Rachel J / Sakuma, Ikki / Yanagimachi, Tsuyoshi / Fujita, Yukihiro / Ugi, Satoshi / Kume, Shinji / Shulman, Gerald I / Maegawa, Hiroshi

    American journal of physiology. Endocrinology and metabolism

    2023  Band 325, Heft 1, Seite(n) E46–E61

    Abstract: Adipose tissues accumulate excess energy as fat and heavily influence metabolic homeostasis. ...

    Abstract Adipose tissues accumulate excess energy as fat and heavily influence metabolic homeostasis.
    Mesh-Begriff(e) Animals ; Mice ; Acetylglucosamine/metabolism ; Fatty Acids, Nonesterified ; Obesity/genetics ; Obesity/metabolism ; Adipose Tissue/metabolism ; Body Weight/genetics ; Weight Gain ; N-Acetylglucosaminyltransferases/genetics ; N-Acetylglucosaminyltransferases/metabolism
    Chemische Substanzen Acetylglucosamine (V956696549) ; Fatty Acids, Nonesterified ; N-Acetylglucosaminyltransferases (EC 2.4.1.-)
    Sprache Englisch
    Erscheinungsdatum 2023-05-24
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 603841-4
    ISSN 1522-1555 ; 0193-1849
    ISSN (online) 1522-1555
    ISSN 0193-1849
    DOI 10.1152/ajpendo.00263.2022
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Ceritinib Aggravates Glycemic Control in Insulin-treated Patients with Diabetes and Metastatic ALK-positive Lung Cancer.

    Sakuma, Ikki / Nagano, Hidekazu / Yoshino, Ichiro / Yokote, Koutaro / Tanaka, Tomoaki

    Internal medicine (Tokyo, Japan)

    2018  Band 58, Heft 6, Seite(n) 817–820

    Abstract: We herein report a 75-year-old woman with insulin-treated diabetes and metastatic anaplastic lymphoma kinase (ALK)-rearranged non-small cell lung cancer who received ceritinib, a second-generation ALK inhibitor, and achieved dramatic tumor reduction. ... ...

    Abstract We herein report a 75-year-old woman with insulin-treated diabetes and metastatic anaplastic lymphoma kinase (ALK)-rearranged non-small cell lung cancer who received ceritinib, a second-generation ALK inhibitor, and achieved dramatic tumor reduction. However, her fasting blood glucose increased, particularly markedly in the first two weeks after ceritinib administration, and did not normalize even increasing the total insulin dose. After discontinuing ceritinib, her glucose levels rapidly reduced. Ceritinib can aggravate hyperglycemia in patients with diabetes who lack compensatory insulin secretion, due to its inhibitory effects on the insulin receptor. Careful monitoring for ceritinib-induced hyperglycemia should be performed, especially in the first two weeks after ceritinib administration.
    Mesh-Begriff(e) Aged ; Anaplastic Lymphoma Kinase/metabolism ; Antineoplastic Agents/adverse effects ; Antineoplastic Agents/therapeutic use ; Biomarkers/blood ; Biomarkers, Tumor/metabolism ; Blood Glucose/metabolism ; Carcinoma, Non-Small-Cell Lung/complications ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/metabolism ; Carcinoma, Non-Small-Cell Lung/pathology ; Diabetes Mellitus, Type 2/blood ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/drug therapy ; Female ; Humans ; Hyperglycemia/blood ; Hyperglycemia/chemically induced ; Hyperglycemia/diagnosis ; Hypoglycemic Agents/therapeutic use ; Insulins/therapeutic use ; Lung Neoplasms/complications ; Lung Neoplasms/drug therapy ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Neoplasm Metastasis ; Pyrimidines/adverse effects ; Pyrimidines/therapeutic use ; Sulfones/adverse effects ; Sulfones/therapeutic use
    Chemische Substanzen Antineoplastic Agents ; Biomarkers ; Biomarkers, Tumor ; Blood Glucose ; Hypoglycemic Agents ; Insulins ; Pyrimidines ; Sulfones ; ALK protein, human (EC 2.7.10.1) ; Anaplastic Lymphoma Kinase (EC 2.7.10.1) ; ceritinib (K418KG2GET)
    Sprache Englisch
    Erscheinungsdatum 2018-11-19
    Erscheinungsland Japan
    Dokumenttyp Case Reports ; Journal Article
    ZDB-ID 32371-8
    ISSN 1349-7235 ; 0021-5120 ; 0918-2918
    ISSN (online) 1349-7235
    ISSN 0021-5120 ; 0918-2918
    DOI 10.2169/internalmedicine.1870-18
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel: Cyclothymic Temperament is Associated with Poor Medication Adherence and Disordered Eating in Type 2 Diabetes Patients: A Case-Control Study.

    Yamamoto, Tetsuya / Sakurai, Kenichi / Watanabe, Masahiro / Sakuma, Ikki / Kanahara, Nobuhisa / Shiina, Akihiro / Hasegawa, Tadashi / Watanabe, Hiroyuki / Iyo, Masaomi / Ishibashi, Ryoichi

    Diabetes therapy : research, treatment and education of diabetes and related disorders

    2021  Band 12, Heft 9, Seite(n) 2611–2624

    Abstract: Introduction: Poor medication adherence and disordered eating are major self-care problems in patients with type 2 diabetes that worsen glycemic control and increase the risk of developing severe diabetes complications. Affective temperament, which ... ...

    Abstract Introduction: Poor medication adherence and disordered eating are major self-care problems in patients with type 2 diabetes that worsen glycemic control and increase the risk of developing severe diabetes complications. Affective temperament, which remains mostly unchanged throughout life, is speculated to predict poor treatment response and high comorbidity. The aim of this study was to explore the link between affective temperament and poor glycemic control due to insufficient self-care.
    Methods: This single-center case-control study involved 77 outpatients divided into the 'poor glycemic control' group (n = 52) and the 'better glycemic control' group (n = 25) based on their mean glycated hemoglobin (HbA1c) levels over the past 12 months. All participants underwent one-on-one interviews during which they completed the following psychometric questionnaires: (1) the Mini-International Neuropsychiatric Interview 5.0.0; (2) the Temperament Evaluation of Memphis, Pisa, and San Diego Auto-questionnaire; (3) a researcher-designed single question for assessing subclinical stress-induced overeating; and (4) the Morisky Medication Adherence Scale. The difference between two continuous independent variables was determined using Student's t test. Discrete variables were compared using the Chi-square (χ
    Results: Those outpatients in the poor glycemic control group exhibited significantly more stress-induced overeating (χ
    Conclusion: Cyclothymic temperament is significantly associated with disordered eating and/or poor medication adherence in patients with type 2 diabetes and is possibly linked to poor glycemic control.
    Sprache Englisch
    Erscheinungsdatum 2021-07-31
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2566702-6
    ISSN 1869-6961 ; 1869-6953
    ISSN (online) 1869-6961
    ISSN 1869-6953
    DOI 10.1007/s13300-021-01121-y
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Identification of genotype-biochemical phenotype correlations associated with fructose 1,6-bisphosphatase deficiency.

    Sakuma, Ikki / Nagano, Hidekazu / Hashimoto, Naoko / Fujimoto, Masanori / Nakayama, Akitoshi / Fuchigami, Takahiro / Taki, Yuki / Matsuda, Tatsuma / Akamine, Hiroyuki / Kono, Satomi / Kono, Takashi / Yokoyama, Masataka / Nishimura, Motoi / Yokote, Koutaro / Ogasawara, Tatsuki / Fujii, Yoichi / Ogawa, Seishi / Lee, Eunyoung / Miki, Takashi /
    Tanaka, Tomoaki

    Communications biology

    2023  Band 6, Heft 1, Seite(n) 787

    Abstract: Fructose-1,6-bisphosphatase (FBPase) deficiency, caused by an FBP1 mutation, is an autosomal recessive disorder characterized by hypoglycemic lactic acidosis. Due to the rarity of FBPase deficiency, the mechanism by which the mutations cause enzyme ... ...

    Abstract Fructose-1,6-bisphosphatase (FBPase) deficiency, caused by an FBP1 mutation, is an autosomal recessive disorder characterized by hypoglycemic lactic acidosis. Due to the rarity of FBPase deficiency, the mechanism by which the mutations cause enzyme activity loss still remains unclear. Here we identify compound heterozygous missense mutations of FBP1, c.491G>A (p.G164D) and c.581T>C (p.F194S), in an adult patient with hypoglycemic lactic acidosis. The G164D and F194S FBP1 mutants exhibit decreased FBP1 protein expression and a loss of FBPase enzyme activity. The biochemical phenotypes of all previously reported FBP1 missense mutations in addition to G164D and F194S are classified into three functional categories. Type 1 mutations are located at pivotal residues in enzyme activity motifs and have no effects on protein expression. Type 2 mutations structurally cluster around the substrate binding pocket and are associated with decreased protein expression due to protein misfolding. Type 3 mutations are likely nonpathogenic. These findings demonstrate a key role of protein misfolding in mediating the pathogenesis of FBPase deficiency, particularly for Type 2 mutations. This study provides important insights that certain patients with Type 2 mutations may respond to chaperone molecules.
    Mesh-Begriff(e) Humans ; Fructose-1,6-Diphosphatase Deficiency/genetics ; Fructose-1,6-Diphosphatase Deficiency/complications ; Fructose-Bisphosphatase/genetics ; Fructose-Bisphosphatase/metabolism ; Fructose ; Acidosis, Lactic/complications ; Acidosis, Lactic/genetics ; Phenotype ; Genotype ; Hypoglycemic Agents
    Chemische Substanzen Fructose-Bisphosphatase (EC 3.1.3.11) ; Fructose (30237-26-4) ; Hypoglycemic Agents
    Sprache Englisch
    Erscheinungsdatum 2023-07-28
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2399-3642
    ISSN (online) 2399-3642
    DOI 10.1038/s42003-023-05160-y
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: Inhibition of

    Luukkonen, Panu K / Sakuma, Ikki / Gaspar, Rafael C / Mooring, Meghan / Nasiri, Ali / Kahn, Mario / Zhang, Xian-Man / Zhang, Dongyan / Sammalkorpi, Henna / Penttilä, Anne K / Orho-Melander, Marju / Arola, Johanna / Juuti, Anne / Zhang, Xuchen / Yimlamai, Dean / Yki-Järvinen, Hannele / Petersen, Kitt Falk / Shulman, Gerald I

    Proceedings of the National Academy of Sciences of the United States of America

    2023  Band 120, Heft 4, Seite(n) e2217543120

    Abstract: Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, in which prognosis is determined by liver fibrosis. A common variant in hydroxysteroid 17-beta dehydrogenase 13 ( ...

    Abstract Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, in which prognosis is determined by liver fibrosis. A common variant in hydroxysteroid 17-beta dehydrogenase 13 (
    Mesh-Begriff(e) Animals ; Humans ; Mice ; Liver/metabolism ; Liver Cirrhosis/pathology ; Non-alcoholic Fatty Liver Disease/pathology ; Pyrimidines/pharmacology ; Pyrimidines/metabolism
    Chemische Substanzen pyrimidine (K8CXK5Q32L) ; Pyrimidines ; HSD17B13 protein, human (EC 1.1.-.-)
    Sprache Englisch
    Erscheinungsdatum 2023-01-20
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2217543120
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: A Unique Case of Renovascular Hypertension due to Fibromuscular Dysplasia in an Extra-renal Artery.

    Sakuma, Ikki / Saito, Jun / Matsuzawa, Yoko / Omura, Masao / Matsui, Seiji / Nishikawa, Tetsuo

    Internal medicine (Tokyo, Japan)

    2018  Band 57, Heft 18, Seite(n) 2689–2694

    Abstract: A 33-year-old man was admitted to our hospital to undergo an evaluation to determine the cause of secondary hypertension. Computerized tomography angiography (CTA) showed bilateral multiple renal arteries with significant stenosis of the right extra- ... ...

    Abstract A 33-year-old man was admitted to our hospital to undergo an evaluation to determine the cause of secondary hypertension. Computerized tomography angiography (CTA) showed bilateral multiple renal arteries with significant stenosis of the right extra-renal artery due to fibromuscular dysplasia and segmental impairment of renal perfusion. Although the plasma aldosterone concentration and plasma renin activity were within the normal ranges, percutaneous balloon dilatation of the stenotic lesion resolved his hypertension, leading to a diagnosis of renovascular hypertension caused by segmental renal ischemia due to extra-renal artery stenosis. CTA should be considered during the examination of patients with early-age hypertension, even if the plasma renin activity is not sufficiently elevated.
    Mesh-Begriff(e) Adult ; Aldosterone/blood ; Angioplasty, Balloon ; Computed Tomography Angiography ; Fibromuscular Dysplasia/blood ; Fibromuscular Dysplasia/complications ; Fibromuscular Dysplasia/diagnostic imaging ; Fibromuscular Dysplasia/therapy ; Humans ; Hypertension, Renovascular/blood ; Hypertension, Renovascular/diagnostic imaging ; Hypertension, Renovascular/etiology ; Male ; Renal Artery Obstruction/blood ; Renal Artery Obstruction/diagnostic imaging ; Renal Artery Obstruction/etiology ; Renal Artery Obstruction/therapy ; Renin/blood
    Chemische Substanzen Aldosterone (4964P6T9RB) ; Renin (EC 3.4.23.15)
    Sprache Englisch
    Erscheinungsdatum 2018-04-27
    Erscheinungsland Japan
    Dokumenttyp Case Reports ; Journal Article
    ZDB-ID 32371-8
    ISSN 1349-7235 ; 0021-5120 ; 0918-2918
    ISSN (online) 1349-7235
    ISSN 0021-5120 ; 0918-2918
    DOI 10.2169/internalmedicine.0023-17
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: MicroRNA-874 targets phosphomevalonate kinase and inhibits cancer cell growth via the mevalonate pathway.

    Aersilan, Alimasi / Hashimoto, Naoko / Yamagata, Kazuyuki / Yokoyama, Masataka / Nakayama, Akitoshi / Shi, Xiaoyan / Nagano, Hidekazu / Sakuma, Ikki / Nohata, Nijiro / Kinoshita, Takashi / Seki, Naohiko / Rahmutulla, Bahityar / Kaneda, Atsushi / Zhahara, Siti Nurul / Gong, Yingbo / Nishimura, Motoi / Kawauchi, Shoichiro / Kawakami, Eiryo / Tanaka, Tomoaki

    Scientific reports

    2022  Band 12, Heft 1, Seite(n) 18443

    Abstract: The microRNA (miR) miR-874, a potential tumour suppressor, causes cell death via target gene suppression in various cancer types. Mevalonate pathway inhibition also causes cell death in breast cancer. However, the relationship between the mevalonate ... ...

    Abstract The microRNA (miR) miR-874, a potential tumour suppressor, causes cell death via target gene suppression in various cancer types. Mevalonate pathway inhibition also causes cell death in breast cancer. However, the relationship between the mevalonate pathway and miR-874-induced apoptosis or its association with the tumour suppressor p53 has not been elucidated. We identified phosphomevalonate kinase (PMVK), a key mevalonate pathway enzyme, and sterol regulatory element-binding factor 2 (SREBF2), the master cholesterol biosynthesis regulator, as direct miR‑874 targets. Next-generation sequencing analysis revealed a significant miR-874-mediated downregulation of PMVK and SREBF2 gene expression and p53 pathway enrichment. Luciferase reporter assays showed that miR-874 directly regulated PMVK and SREBF2. miR-874-induced apoptosis was p53 dependent, and single-cell RNA sequencing analysis demonstrated that miR-874 transfection resulted in apoptosis and p53 pathway activation. Downregulation of PMVK expression also caused cell cycle arrest and p53 pathway activation, which was rescued by geranylgeranyl pyrophosphate (GGPP) supplementation. Analysis of The Cancer Genome Atlas (TCGA) database indicated a negative correlation between miR-874 and PMVK expression and between miR-874 and SREBF2 expression. These findings suggest that miR-874 suppresses the mevalonate pathway by targeting SREBF2 and PMVK, resulting in GGPP depletion, which activates the p53 pathway and promotes cycle arrest or apoptosis.
    Mesh-Begriff(e) Humans ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Mevalonic Acid/metabolism ; Cell Line, Tumor ; MicroRNAs/metabolism ; Apoptosis/genetics ; Cell Transformation, Neoplastic/genetics ; Cell Proliferation/genetics ; Gene Expression Regulation, Neoplastic
    Chemische Substanzen MIRN874 microRNA, mouse ; Tumor Suppressor Protein p53 ; Mevalonic Acid (S5UOB36OCZ) ; phosphomevalonate kinase (EC 2.7.4.2) ; MicroRNAs ; MIRN874 microRNA, human
    Sprache Englisch
    Erscheinungsdatum 2022-11-02
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-022-23205-w
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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