Small nucleolar RNAs and long non-coding RNAs of the SNHG family in the pathogenesis of ovarian cancer

Мұқаба

Дәйексөз келтіру

Толық мәтін

Ашық рұқсат Ашық рұқсат
Рұқсат жабық Рұқсат берілді
Рұқсат жабық Рұқсат ақылы немесе тек жазылушылар үшін

Аннотация

The discovery of a class of long non-coding RNAs (lncRNAs), including lncRNAs of the small nucleolar RNA (snoRNA) host gene family — SNHG, has led to growing interest in the study of both snoRNAs themselves and the genes encoding them. Currently, of the 232 known snoRNA genes, only 32 have been confirmed to have lncRNAs. At the same time, a positive correlation has been shown between the expression of lncRNAs and snoRNAs encoded by a common host gene of the SNHG family. Thus, lncRNA of the SNHG1 gene correlates with snoRNAs SNORD22, SNORD25–31, and lncRNA of the SNHG16 gene — with snoRNAs SNORD1A, SNORD1B and SNORD1C. There is evidence that SNHG lncRNAs can participate in oncogenesis both through regulatory functions inherent to lncRNAs and by influencing ribosome biogenesis. At the same time, information has accumulated on the “extraribosomal” functions of snoRNAs. In addition to a brief excursion into the biological functions of snoRNAs and SNHG lncRNAs, we present a comprehensive review of data on the role of these two types of non-coding RNAs in the pathogenesis of ovarian cancer, the most insidious cancer of the female reproductive system. The influence of these regulatory RNAs on the main processes of ovarian oncogenesis, such as apoptosis, epithelial-mesenchymal transition, cell cycle control, and DNA methylation mechanisms in this type of cancer is considered. The prospects for clinical application of regulatory RNAs due to their influence on the level of drug resistance are also discussed.

Толық мәтін

Рұқсат жабық

Авторлар туралы

А. Burdennyy

Research Institute of General Pathology and Pathophysiology; N.M. Emanuel Institute of Biochemical Physics, Russian Academy of Sciences

Хат алмасуға жауапты Автор.
Email: burdennyy@gmail.com
Ресей, Moscow, 125315; Moscow, 119334

V. Loginov

Research Institute of General Pathology and Pathophysiology; N.P. Bochkov Medical Genetic Research Center

Email: burdennyy@gmail.com
Ресей, Moscow, 125315; Moscow, 115522

M. Fridman

N.I. Vavilov Institute of General Genetics, Russian Academy of Sciences

Email: burdennyy@gmail.com
Ресей, Moscow, 117971

N. Kushlinskii

N.N. Blokhin National Medical Research Center of Oncology, Ministry of Health of the Russian Federation

Email: burdennyy@gmail.com
Ресей, Moscow, 115522

E. Braga

Research Institute of General Pathology and Pathophysiology; N.P. Bochkov Medical Genetic Research Center

Email: eleonora10_45@mail.ru
Ресей, Moscow, 125315; Moscow, 115522

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2. Fig. 1. Processes involving snoRNAs (a) and lncRNAs of the SNHG family (b) (taken from [7] with modifications by the authors, Creative Commons Attribution License (CC BY)).

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3. Fig. 2. Axis of SNHG20 interactions with the oncoprotein ROCK1 mediated by microRNAs in ovarian cancer progression. SNHG20 (red), as an initial factor with increased expression, is involved in ovarian cancer progression. SNHG20 binds to and suppresses the expression of miR-148a (blue), which is a key step in the mechanism of tumor progression. Suppression of miR-148a leads to an increase in the expression of the transcription factor ROCK1 (green). ROCK1, in turn, activates cell proliferation and invasion processes, and suppresses apoptosis (blue). All these processes together contribute to the progression of ovarian cancer (yellow).

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4. Fig. 3. Scheme of interactions of SNHG16 lncRNA in ovarian cancer (OC) cells leading to tumor progression and drug resistance.

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