Potentiation of the malignant phenotype of the undifferentiated ARO thyroid cell line by insertion of thebcl-2 gene

Basolo, Fulvio; Fiore, Lisa B.; Giannini, Raffaello; Albini, Adriana; Merlo, Giorgio R.; Fontanini, Gabriella; Conaldi, Pier Giulio; Toniolo, Antonio

doi:10.1002/(sici)1097-0215(19990611)81:6<956::aid-ijc19>3.0.co;2-n

Cited by 15 publications

(8 citation statements)

References 13 publications

(2 reference statements)

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“…Indeed, the effects of Bcl-2 on anchorageindependent growth are controversial. Bcl-2 overexpression has been shown to be sufficient to allow anchorage-independent growth in bladder or thyroid tumor cells and to protect against ␥ irradiation-induced loss of clonogenic potential (Basolo et al, 1999;Miyake et al, 1999). On the other hand, in leukemic cells, overexpression of Bcl-2 or Bcl-x L could not prevent Ara-C-or paclitaxel-induced loss of clonogenicity (Wang et al, 1999;Tang et al, 2000).…”

Section: Resultsmentioning

confidence: 99%

“…For example, Bcl-2 inhibits apoptosis induced by a variety of stimuli, and its overexpression can also induce transformation of cells resulting in increased clonogenicity and tumor growth (Basolo et al, 1999;Miyake et al, 1999). However, Bcl-2 overexpression inhibited apoptosis but did not prevent loss of anchorage-independent growth caused by 1-␤-D-arabinofuranosylcytosine (Ara-C) or paclitaxel (Wang et al, 1999;Tang et al, 2000).…”

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confidence: 99%

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Inhibition of Protein Kinase Cα Enhances Anticancer Agent-Induced Loss of Anchorage-Independent Growth Regardless of Protection against Apoptosis by Bcl-2

Huigsloot

Tijdens²,

Water³

2003

Mol Pharmacol

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

Inhibition of Protein Kinase Cα Enhances Anticancer Agent-Induced Loss of Anchorage-Independent Growth Regardless of Protection against Apoptosis by Bcl-2

Huigsloot

Tijdens²,

Water³

2003

Mol Pharmacol

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“…In addition, HMGA2 derepresses the expression of Bcl-2 by inhibiting miR-34a, thereby promoting an anti-apoptotic pathway (91). In thyroid cells overexpressing Bcl-2 by infection with a Bcl-2 retroviral vector, the expression of HMGA2 was correspondingly increased and apoptosis was inversely decreased (93). The PI3K/Akt signalling pathway is always hyperactivated in human cancer, which is a key contributor to resistance to apoptosis (94).…”

Section: Dual Role Of Hmga2 In Apoptosismentioning

confidence: 99%

Oncological role of HMGA2 (Review)

2019

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The high mobility group A2 (HMGA2) protein is a non-histone architectural transcription factor that modulates the transcription of several genes by binding to AT-rich sequences in the minor groove of B-form DNA and alters the chromatin structure. As a result, HMGA2 influences a variety of biological processes, including the cell cycle process, DNA damage repair process, apoptosis, senescence, epithelial-mesenchymal transition and telomere restoration. In addition, the overexpression of HMGA2 is a feature of malignancy, and its elevated expression in human cancer predicts the efficacy of certain chemotherapeutic agents. Accumulating evidence has suggested that the detection of HMGA2 can be used as a routine procedure in clinical tumour analysis. Contents 1. Introduction 2. Regulation of the expression of HMGA2 3. Expression of HMGA2 in cancer 4. HMGA2 influences the cell cycle of cancer cells 5. HMGA2 and the DNA damage response 6. Dual role of HMGA2 in the regulation of non-homologous end-joining 7. HMGA2 promotes base excision repair 8. HMGA2 promotes nucleotide excision repair 9. Apoptosis 10. Dual role of HMGA2 in apoptosis 11. HMGA2 impairs or enhances cellular senescence 12. HMGA2 promotes epithelial-mesenchymal transition 13. HMGA2 maintains telomere length 14. HMGA2 predicts the efficacy of chemotherapy 15. Considerations and perspectives Hangzhou, Zhejiang 310014;

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“… 7,13,14 Such basement‐membrane organization appears to actively maintain thyroid‐follicle structures through stability of thyrocyte integration. Matrigel (Collaborative Research, Bedford, MA, USA) can also be applied in 3‐D gel culture, 41–45 although its strength is weaker than that of type I collagen gel. Type I collagen can be mixed with various ECM molecules or cytokines in a 3‐D culture system (unpublished data).…”

Section: Thyrocyte Integration In a 3‐d Collagen Gel Culture Systemmentioning

confidence: 99%

Thyrocyte integration, and thyroid folliculogenesis and tissue regeneration: Perspective for thyroid tissue engineering

Toda¹,

Koike²,

Sugihara³

2001

Pathology International

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The thyroid gland is composed of many ball-like structures called thyroid follicles, which are supported by the interfollicular extracellular matrix (ECM) and a capillary network. The component thyrocytes are highly integrated in their specific structural and functional polarization. In conventional monolayer and floating culture systems, thyrocytes cannot organize themselves into follicles with normal polarity. In contrast, in 3-D collagen gel culture, thyrocytes easily form stable follicles with physiological polarity. Integration of thyrocyte growth and differentiation results ultimately in thyroid folliculogenesis. This culture method and subacute thyroiditis are two promising models for addressing mechanisms of folliculogenesis, because thyroid-follicle formation actively occurs both in the culture system and at the regenerative phase of the disorder. The understanding of the mechanistic basis of folliculogenesis is prerequisite for generation of artificial thyroid tissue, which would enable a more physiological strategy to the treatment of hypothyroidism caused by various diseases and surgical processes than conventional hormone replacement therapy. We review here thyrocyte integration, and thyroid folliculogenesis and tissue regeneration. We also briefly discuss a perspective for thyroid tissue regeneration and engineering.

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Potentiation of the malignant phenotype of the undifferentiated ARO thyroid cell line by insertion of thebcl-2 gene

Cited by 15 publications

References 13 publications

Inhibition of Protein Kinase Cα Enhances Anticancer Agent-Induced Loss of Anchorage-Independent Growth Regardless of Protection against Apoptosis by Bcl-2

Inhibition of Protein Kinase Cα Enhances Anticancer Agent-Induced Loss of Anchorage-Independent Growth Regardless of Protection against Apoptosis by Bcl-2

Oncological role of HMGA2 (Review)

Thyrocyte integration, and thyroid folliculogenesis and tissue regeneration: Perspective for thyroid tissue engineering

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