Reverse transcriptase inhibitors reduce tumor growth in vivo and induce cell differentiation

Landriscina, Matteo; Quirino, Michela; Sciamanna, Ilaria; Pittoggi, Carmine; D’Argento, Ettore; Schinzari, G.; Leonardo, Gabriella Di; Cassano, A; Spadafora, Corrado; Barone, C.

doi:10.1200/jco.2004.22.90140.3134

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“…PCNA has been involved in DNA replication and repair, reflecting cell proliferation . Bax is a proapoptotic protein that can induce apoptosis, while Bcl‐2 is an antiapoptotic factor inhibiting cell apoptosis, and Cyclin D1 controls the induction of the G1 phase of the cell cycle . The aforementioned results indicated that miR‐329 inhibited PTTG1, subsequently inhibiting the MAPK signaling pathway, thereby enabling the modulation of cell proliferation, apoptosis, and cell cycle arrest.…”

Section: Resultsmentioning

confidence: 99%

MicroRNA‐329‐mediated PTTG1 downregulation inactivates the MAPK signaling pathway to suppress cell proliferation and tumor growth in cholangiocarcinoma

Zheng

et al. 2018

J of Cellular Biochemistry

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Cholangiocarcinoma (CCA) is a severe malignancy usually producing a poor prognosis and high mortality rate. MicroRNAs (miRNAs) have been reported in association with CCA; however, the role miR-329 plays in the CCA condition still remains unclear. Therefore, this study was conducted to explore the underlying mechanism of which miR-329 is influencing the progression of CCA. This work studied the differential analysis of the expression chips of CCA obtained from the Gene Expression Omnibus database. Next, to determine both the expression and role of pituitary tumor transforming gene-1 (PTTG1) in CCA, the miRNAs regulating PTTG1 were predicted. In the CCA cells that had been intervened with miR-329 upregulation or inhibition, along with PTTG1 silencing, expression of miR-329, PTTG1, p-p38/p38, p-ERK5/ERK5, proliferating cell nuclear antigen (PCNA), Cyclin D1, Bcl-2-associated X protein (Bax), B-cell CLL/lymphoma 2 (Bcl-2), and caspase-3 were determined. The effects of both miR-329 and PTTG1 on cell proliferation, cell-cycle distribution, and apoptosis were also assayed. The miR-329 was likely to affect the CCA development through regulation of the PTTG1-mediated mitogen-activated protein kinase (MAPK) signaling pathway.The miR-329 targeted PTTG1, leading to inactivation of the MAPK signaling pathway. Upregulation of miR-329 and silencing of PTTG1 inhibited the CCA cell proliferation, induced cell-cycle arrest, and subsequently promoted apoptosis with elevations in Bax, cleaved caspase-3, and total caspase-3, but showed declines in PCNA, Cyclin D1, and Bcl-2. Moreover, miR-329 was also found to suppress the tumor growth by downregulation of PTTG1. To summarize, miR-329 inhibited the expression of PTTG1 to inactivate the MAPK signaling pathway, thus suppressing the CCA progression, thereby providing a therapeutic basis for the CCA treatment. K E Y W O R D S cholangiocarcinoma, microRNA-329, mitogen-activated protein kinase signaling pathway, pituitary tumor transforming gene-1, tumor growth J Cell Biochem. 2019;120:9964-9978. wileyonlinelibrary.com/journal/jcb 9964 |

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Section: Resultsmentioning

confidence: 99%

MicroRNA‐329‐mediated PTTG1 downregulation inactivates the MAPK signaling pathway to suppress cell proliferation and tumor growth in cholangiocarcinoma

Zheng

et al. 2018

J of Cellular Biochemistry

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show abstract

Reverse transcriptase inhibitors reduce tumor growth in vivo and induce cell differentiation

Cited by 1 publication

References 0 publications

MicroRNA‐329‐mediated PTTG1 downregulation inactivates the MAPK signaling pathway to suppress cell proliferation and tumor growth in cholangiocarcinoma

MicroRNA‐329‐mediated PTTG1 downregulation inactivates the MAPK signaling pathway to suppress cell proliferation and tumor growth in cholangiocarcinoma

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