Role of STAT3 Transcription Factor in Pathogenesis of Bronchial Asthma

Nikolskii, A.A.; Shilovskiy, Igor; Barvinskaia, Ekaterina; Korneev, A.V.; Sundukova, Maria; Khaitov, Musa

doi:10.1134/s0006297921110122

Cited by 17 publications

(14 citation statements)

References 84 publications

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“…the STAT3 gene encodes the STAT family transcription factor mediating the cellular responses to interleukins and regulates the inflammatory response [ 45 , 46 ];…”

Section: Discussionmentioning

confidence: 99%

“…TBX21, TBX5 кодируют белки -факторы активации транскрипции, экспрессия этих факторов снижена в T-клетках дыхательных путей больных астмой [16,44]; STAT6 кодирует фактор активации транскрипции семейства STAT; экспрессия этого гена значительно повышена у больных тяжелой формой БА [16]; ген STAT3 кодирует фактор активации транскрипции семейства STAT, который опосредует клеточные ответы на интерлейкины и действует как регулятор воспалительного ответа [45,46]; STAT4 кодирует фактор активации транскрипции семейства STAT, экспрессия этого гена снижена у больных БА [47];…”

Section: Discussionunclassified

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Genetic Variants Associated with Bronchial Asthma Specific to the Population of the Russian Federation

et al. 2023

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Bronchial asthma (BA) is a disease that still lacks an exhaustive treatment protocol. In this regard, the global medical community pays special attention to the genetic prerequisites for the occurrence of this disease. Therefore, the search for the genetic polymorphisms underlying bronchial asthma has expanded considerably. As the present study progressed, a significant amount of scientific medical literature was analyzed and 167 genes reported to be associated with the development of bronchial asthma were identified. A group of participants (n = 7,303) who had voluntarily provided their biomaterial (venous blood) to be used in the research conducted by the Federal Medical Biological Agency of Russia was formed to subsequently perform a bioinformatic verification of known associations and search for new ones. This group of participants was divided into four cohorts, including two sex-distinct cohorts of individuals with a history of asthma and two sex-distinct cohorts of apparently healthy individuals. A search for polymorphisms was made in each cohort among the selected genes, and genetic variants were identified whose difference in occurrence in the different cohorts was statistically significant (significance level less than 0.0001). The study revealed 11 polymorphisms that affect the development of asthma: four genetic variants (rs869106717, rs1461555098, rs189649077, and rs1199362453), which are more common in men with bronchial asthma compared to apparently healthy men; five genetic variants (rs1923038536, rs181066119, rs143247175, rs140597386, and rs762042586), which are more common in women with bronchial asthma compared to apparently healthy women; and two genetic variants (rs1219244986 and rs2291651) that are rare in women with a history of asthma.

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“…the STAT3 gene encodes the STAT family transcription factor mediating the cellular responses to interleukins and regulates the inflammatory response [ 45 , 46 ];…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionunclassified

Genetic Variants Associated with Bronchial Asthma Specific to the Population of the Russian Federation

et al. 2023

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“…This study investigated the influence of different solvent ratios (water, 50% methanol, and methanol) on the sample analysis results. It was observed that the characteristic chromatographic profile obtained with its activity dependent on the presence of macrophages, neutrophils, and cytokines such as interleukin-6 (Nikolskii et al, 2021). Studies have shown that STAT3 plays a vital role in airway smooth muscle proliferation, and inhibiting its expression can reduce airway smooth muscle cell proliferation in patients with asthma (Nishimura et al, 2022;Xue et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

“…Based on the results of network pharmacology analysis, it is evident that CGP, containing seven active components including sinapine thiocyanate and ephedrine hydrochloride, targets key proteins in the treatment of bronchial asthma, including STAT3 (signal transducer and activator of transcription 3), TP53 (tumor protein P53), and MAPK3 (mitogen‐activated protein kinase 3), among others. STAT3, as a crucial transcription factor, participates in the regulation of lung inflammation, with its activity dependent on the presence of macrophages, neutrophils, and cytokines such as interleukin‐6 (Nikolskii et al, 2021). Studies have shown that STAT3 plays a vital role in airway smooth muscle proliferation, and inhibiting its expression can reduce airway smooth muscle cell proliferation in patients with asthma (Nishimura et al, 2022; Xue et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Prediction and analysis of quality markers for Chuantieling gel patches based on HPLC fingerprinting and network pharmacology

Du,

Lu,

Xiao

et al. 2023

Biomedical Chromatography

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The Chuantieling gel patch (CGP), a traditional Chinese medicine compound, is an external treatment for asthma. It has shown remarkable effectiveness in alleviating asthma‐related airway hyperresponsiveness and inflammation. Nevertheless, there is currently no information available regarding the analysis of quality markers for CGP, and there is a need for further improvement in quality control research. In this study, we developed an HPLC fingerprinting method for CGP and conducted a comprehensive methodological investigation. We assessed the similarity among 10 batches of CGP, identified common peaks, and quantified the content of seven major quality markers. Furthermore, we built a network pharmacology–based ‘active ingredients–targets–pathways–diseases’ network to forecast the potential mechanisms of action for the primary active components in asthma treatment. Our findings demonstrated that the developed CGP fingerprinting and content determination methods were consistent and trustworthy. We verified the existence of 25 shared peaks and successfully identified 7 chromatographic peaks, including sinigrin thiocyanate, ephedrine hydrochloride, methyleugenol, imperatorin, cinnamaldehyde, emodin, and 6‐gingerol, using reference standards. The network pharmacology analysis suggested that these seven active components may target proteins such as STAT3 (signal transducer and activator of transcription 3), MAPK3 (mitogen‐activated protein kinase 3), and TP53 (tumor protein P53) and influence various diseases through pathways including cancer pathways, hepatitis B, and PI3K–Akt (phosphoinositide 3‐kinase–protein kinase B) signaling. This study provides insight into the complex multicomponent composition of CGP, and the predictive analysis through network pharmacology sets the stage for uncovering the mechanisms responsible for the therapeutic effects of CGP.

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“…Initially identified as an IL-6-induced acute phase response protein, STAT3 has been extensively investigated and is reported to participate in many physiological and pathological processes [22][23][24][25][26][27]. It is known that, in oncology, signals mediated by STAT3 contribute to the onset and progression of malignancies [27].…”

Section: Discussionmentioning

confidence: 99%

KDF1 Promoted Proliferation, Migration and Invasion of Lung Adenocarcinoma Cells through Activating STAT3 and AKT Pathway

Guo,

Gan,

Bao

et al. 2023

Biomedicines

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KDF1 has been reported to be correlated with carcinogenesis. However, its role and mechanism are far from clear. To explore the possible role and underlying mechanism of KDF1 in lung adenocarcinoma (LUAD), we investigated KDF1 expression in LUAD tissues and the influence of KDF1 in the phenotype of LUAD cells (A549 and PC-9) as well as the underlying mechanism. Compared to non-tumor lung epithelial cells, KDF1 was upregulated in the cancer cells of the majority of LUAD patients, and its expression was correlated with tumor size. Patients with enhanced KDF1 in cancer cells (compared with paired adjacent non-neoplastic lung epithelial cells) had shorter overall survival than patients with no increased KDF1 in cancer cells. Knockdown of KDF1 inhibited the migration, proliferation and invasion of LUAD cells in vitro. And overexpression of KDF1 increased the growth of the subcutaneous tumors in mice. In terms of molecular mechanisms, overexpression of KDF1 induced the expression of AKT, p-AKT and p-STAT3. In KDF1-overexpressing A549 cells, inhibition of the STAT3 pathway decreased the level of AKT and p-AKT, whereas inhibition of the AKT pathway had no effect on the activation of STAT3. Inhibition of STAT3 or AKT pathways reversed the promoting effects of KDF1 overexpression on the LUAD cell phenotype and STAT3 inhibition appeared to have a better effect. Finally, in the cancer cells of LUAD tumor samples, the KDF1 level was observed to correlate positively with the level of p-STAT3. All these findings suggest that KDF1, which activates STAT3 and the downstream AKT pathway in LUAD, acts as a tumor-promoting factor and may represent a therapeutic target.

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Role of STAT3 Transcription Factor in Pathogenesis of Bronchial Asthma

Cited by 17 publications

References 84 publications

Genetic Variants Associated with Bronchial Asthma Specific to the Population of the Russian Federation

Genetic Variants Associated with Bronchial Asthma Specific to the Population of the Russian Federation

Prediction and analysis of quality markers for Chuantieling gel patches based on HPLC fingerprinting and network pharmacology

KDF1 Promoted Proliferation, Migration and Invasion of Lung Adenocarcinoma Cells through Activating STAT3 and AKT Pathway

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