In the original publication [], the following three references, [26,74,76], should be replaced with new references. References [26] and [74] were replaced because the articles were retracted, and reference [76] was replaced because of a citation error. With this correction, the order of some references, the contents of Table 1, and the third paragraph of Section 4 in the article have also been modified accordingly. The authors state that the scientific conclusions are unaffected. This correction was approved by the Academic Editor. The original publication has also been updated.
The corrected references that replaced references [26], [74], and [76] are as follows:
- 26. Zhu, D.; Xiao, Z.; Wang, Z.; Hu, B.; Duan, C.; Zhu, Z. MEG3/MIR-376B-3P/HMGA2 axis is involved in pituitary tumor invasiveness. J. Neurosurg. 2020, 134, 499–511. https://doi.org/10.3171/2019.10.JNS191959.
- 74. Shahrzad, J.; Monsalves, E.; Tateno, T.; Zadeh, G. Role of mTOR inhibitors in growth hormone-producing pituitary adenomas harboring different FGFR4 genotypes. Endocrinology 2016, 157, 3577–3587.
- 76. Bin, H.; Mao, Z.; Du, Q.; Jiang, X.; Wang, Z.; Xiao, Z.; Zhu, D.; Wang, X.; Zhu, Y.; Wang, H. miR-93-5p targets Smad7 to regulate the transforming growth factor-β1/Smad3 pathway and mediate fibrosis in drug-resistant prolactinoma. Brain Res. Bull. 2019, 149, 21–31.
The corrected version of Table 1 is as follows:
Table 1.
Experimental information on miRNAs involved in the tumorigenesis of pituitary adenomas and their target genes by tumor type.
Table 1.
Experimental information on miRNAs involved in the tumorigenesis of pituitary adenomas and their target genes by tumor type.
| miRNA | Gene Target | Type of PA | Biological Function | Regulation | Phenotype | Ref. |
|---|---|---|---|---|---|---|
| miR-524-5p | PTTG1/PBF | NFA | Inhibition of tumor cell proliferation, migration, and invasion | Down | Tumor suppressor | [19] |
| miR-424, miR-503 | CDC25A | NFA | Inhibition of tumor cell growth | Down | Tumor suppressor | [20] |
| miR-34 | AIP | GH | Induces invasive properties in tumor cells | Up | OncomiR | [21] |
| miR-410 | CCNB1 | FSH/LH | Increased expression of cyclin A and D protein affecting the G1-S phase of the cell cycle; inhibition of tumor cell proliferation | Down | Tumor suppressor | [22] |
| miR-26a | PLAG1 | NFA, GH, ACTH, PRL | Induces invasive properties in tumor cells | Up | OncomiR | [23] |
| miR-23b | HMGA2 | NFA, FSH/LH, GH | Inhibition of tumor cell proliferation, delaying cell division in the G1 phase of the cell cycle | Down | Tumor suppressor | [24] |
| miR-130b | CCNA2 | NFA, FSH/LH, GH | Inhibition of tumor cell proliferation, delaying cell division in the G2 phase of the cell cycle | Down | Tumor suppressor | [24] |
| miR-106b | PTEN | Invasive (NFA, GH, ACTH, PRL) | Induces invasive properties in tumor cells | Up | OncomiR | [25] |
| MIR-376B-3P with MEG3 | HMGA2 | Clinical nonfunctioning pituitary adenomas (CNFPAs) | HMGA2, acting as a target gene of MIR-376B-3P, functions as an oncogene in PA and can be downregulated by MEG3 through the accumulation of MIR-376B-3P | - | Tumor suppressor | [26] |
| miR-132, miR-15a, miR-16 | SOX5 | Invasive (NFA, GH, ACTH, PRL) | Inhibition of tumor cell proliferation, migration, and invasion | Down | Tumor suppressor | [27] |
| miR-200c | PTEN | PRL | Tumor cell apoptosis reduction | Up | OncomiR | [28] |
| miR-329, miR-300, miR-381, miR-655 | PTTG1 | PRL, GH | Inhibition of tumor cell growth | Down | Tumor suppressor | [29] |
| miR-20a, miR-17-5p | PTEN, TIMP2 | NFA | Carcinoma metastasis | Up | OncomiR | [27] |
| miR-106b | PTEN-PI3K/AKT | NFA | Activation of invasive properties and migration of tumor cells; carcinoma metastasis | Up | OncomiR | [27,30] |
| miR-183 | KIAA0101 | PRL | Inhibition of tumor cell proliferation | Down | Tumor suppressor | [31] |
| miR-15, miR-16, miR-26a, miR-196a2, Let-7a | HMGA1, HMGA2 | GH, PRL | Inhibition of tumor cell proliferation | Up | Tumor suppressor | [32] |
NFA, nonfunctioning adenoma; GH, growth hormone-secreting adenoma; FSH, follicle-stimulating hormone adenoma; LH, luteinizing hormone-secreting adenoma; ACTH, adrenocorticotropic hormone-secreting adenoma; PRL, prolactin-secreting adenoma; PTTG1IP, pituitary tumor-transforming 1 interacting protein; PBF, pituitary tumor-transforming gene binding factor; CDC25A, cell division cycle 25 A; AIP, aryl hydrocarbon receptor-interacting protein; CCNB1, G2/mitotic-specific cyclin-B1; PLAG1, pleomorphic adenoma gene 1; HMGA1, high-mobility group AT-hook 1; HMGA2, high-mobility group AT-hook 2; CCNA2, cyclin A2; PTEN, phosphatase and tensin homolog deleted on chromosome 10; AKT3, serine/threonine kinase 3; SOX5, SRY-related HMG-box; SSTR2, somatostatin receptor type 2; TIMP2, tissue inhibitor of metalloproteinases 2; PI3K, phosphoinositide 3-kinases; KIAA0101, protein; miR, microRNA; PA, pituitary adenoma.
The correct contents of the third paragraph of Section 4 are as follows:
mTOR is a serine–threonine specificity protein kinase that controls cell growth and metabolism in response to various substances, growth factors, and cell stress [71]. As a central regulator of cell growth, mTOR plays a key role in the development and aging of cells and is involved in the pathogenesis of cardiovascular diseases, endocrine diseases, metabolic disorders, and tumors [72]. Antiproliferative responses to mTOR inhibition have been reported in studies with aggressive PA in vitro and in vivo [73,74]. mTOR mRNA expressions significantly modulated in invasive pituitary adenoma tissues were compared with those in noninvasive pituitary adenoma tissues [73,74].
Reference
- Beylerli, O.; Beeraka, N.M.; Gareev, I.; Pavlov, V.; Yang, G.; Liang, Y.; Aliev, G. MiRNAs as Noninvasive Biomarkers and Therapeutic Agents of Pituitary Adenomas. Int. J. Mol. Sci. 2020, 21, 7287. [Google Scholar] [CrossRef] [PubMed]
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