The role of MMP-1 and FGFR4-R388 gene polymorphisms in pituitary adenoma

Zlatkutė, Eglė; Liutkevičienė, Rasa; Vilkeviciute, Alvita; Glebauskiene, Brigita; Kriauciuniene, Loresa; Jakštienė, Silvija; Žaliūnienė, Dalia

doi:10.6001/actamedica.v24i4.3613

Cited by 3 publications

(3 citation statements)

References 38 publications

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“…PA account for 10%‐15% of all intracranial tumors . Although most PA are histologically benign tumors, their location in the brain makes them very serious .…”

Section: Discussionmentioning

confidence: 99%

Reduction of miR‐212 contributes to pituitary adenoma cell invasion via targeting c‐Met

Wang

Gao

2019

The Kaohsiung J of Med Scie

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The current study aimed to evaluate the expression and role of miR-212 in the progression of pituitary adenoma (PA), thereby providing a theoretical basis and potential therapy methods for PA patients. Our data showed that miR-212 levels were significantly reduced in PA tissues than normal pituitary tissues. However, no significant difference was identified in the serum of PA patients and healthy control. In addition, the expression of miR-212 in invasive PA was significantly lower than that in noninvasive and normal pituitary tissues. Moreover, the level of miR-212 was decreased with the increase of tumor invasion. Meanwhile, the expression of miR-212 in giant adenomas was significantly lower than that in macroadenomas and microadenomas. Furthermore, inhibition of miR-212 significantly enhanced the proliferation and invasive capacity of GH3 cells. Dual luciferase reporter assay and western blot analysis confirmed that c-Met was a target gene of miR-212. More importantly, upregulation of c-Met significantly prompted PA cell proliferation mainly as a result of the enhanced level of phosphorylation of AKT. This effect could be abolished when c-Met was silenced in GH3 cells. In summary, reduced miR-212 expression in PA contributed to abnormal cancer cell proliferation and invasion mainly by targeting c-Met.

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“…PA account for 10%‐15% of all intracranial tumors . Although most PA are histologically benign tumors, their location in the brain makes them very serious .…”

Section: Discussionmentioning

confidence: 99%

Reduction of miR‐212 contributes to pituitary adenoma cell invasion via targeting c‐Met

Wang

Gao

2019

The Kaohsiung J of Med Scie

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“…Thus, PAs exhibiting high MMP activity can be associated with aggressive tumor phenotype. Zlatkute et al (2017) discussed the role of MMP-1 polymorphisms on the development of PAs by analyzing genetic profiles of 100 patients with PA and comparing them with healthy controls [20]. They found that the polymorphism in the MMP-1 gene 1G/1G was more frequent in the invasive group of PAs and in the more active tumors than in control PAs (p = 0.044), suggesting that this polymorphism may play a role in PA development [20].…”

Section: Snps Found In Pas In General (Functional and Nonfunctional)mentioning

confidence: 99%

“…Zlatkute et al (2017) discussed the role of MMP-1 polymorphisms on the development of PAs by analyzing genetic profiles of 100 patients with PA and comparing them with healthy controls [20]. They found that the polymorphism in the MMP-1 gene 1G/1G was more frequent in the invasive group of PAs and in the more active tumors than in control PAs (p = 0.044), suggesting that this polymorphism may play a role in PA development [20]. This was in contrast to a previous paper by Atlas et al (2010), in which they found that MMP-1 2G/2G alleles were more common in the invasive PAs than 1G/1G variants, but that allelic pattern was not statistically significant compared with control [21].…”

Section: Snps Found In Pas In General (Functional and Nonfunctional)mentioning

confidence: 99%

The Role of Single-Nucleotide Polymorphisms in Pituitary Adenomas Tumorigenesis

Shah

Aghi

2019

Cancers

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Pituitary adenomas (PAs) are among the most common intracranial neoplasms, but despite their histologically benign nature, these tumors sometimes grow large enough to cause symptoms of mass effect such as vision loss, headaches, or hypopituitarism. When they get this large, surgery will unfortunately not be curative and, other than prolactinomas, medical options are limited, and radiation has variable efficacy in controlling growth. Understanding the genetic perturbations, such as single nucleotide polymorphisms (SNPs), that promote the formation or growth of functional and nonfunctional PAs is important because such genetic insights could improve the diagnosis and subsequent classification of PAs as well as unlock potential therapeutic targets outside contemporary standard of care. While there have been great strides in the research of SNPs as drivers of PA formation and maintenance, a comprehensive discussion of these genetic mutations has not been undertaken. In the present article, and with the goal of providing scientists and clinicians a central review, we sought to summarize the current literature on SNPs and their relationship to PA formation. Across multiple tumor types, such as nonfunctioning PAs, prolactinomas, corticotroph adenomas, somatotroph adenomas, thyrotropic adenomas, and gonadotroph adenomas, SNPs in cell surface receptors implicated in proliferation can be appreciated. Polymorphisms found in tumor suppressors and cell cycle regulators have also been identified, such as p53 SNPs in nonfunctioning PAs or cyclin D1 in prolactinomas. While the translational relevance of SNPs in the formation of PAs is still in the early stages, the use of wide-scale genomic analysis to identify patients at risk for developing PAs could yield therapeutic benefit in the future.

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