DNA methyltransferase inhibitors influence on the DIRAS3 and STAT3 expression and in vitro migration of ovarian and breast cancer cells

Nowak, Ewa; Poczęta, Marta; Bieg, Dominik; Bednarek, Ilona

doi:10.5603/gp.a2017.0099

Cited by 11 publications

(9 citation statements)

References 25 publications

(32 reference statements)

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“…Previous studies have demonstrated that DNA methylation and chromatin modulation may also be regulated by STAT-3 via epigenetic mechanisms (17,18). Moreover, STAT-3 has been recognized as a potent immune checkpoint regulator for…”

Section: Introductionmentioning

confidence: 99%

Overview of the STAT‑3 signaling pathway in cancer and the development of specific inhibitors (Review)

Mohammad

Liu

2020

Oncol Lett

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Signal transducer and activator of transcription (STAT) proteins represent novel therapeutic targets for the treatment of cancer. In particular, STAT-3 serves critical roles in several cellular processes, including the cell cycle, cell proliferation, cellular apoptosis and tumorigenesis. Persistent activation of STAT-3 has been reported in a variety of cancer types, and a poor prognosis of cancer may be associated with the phosphorylation level of STAT-3. Furthermore, elevated STAT-3 activity has been demonstrated in a variety of mammalian cancers, both in vitro and in vivo. This indicates that STAT-3 serves an important role in the progression of numerous cancer types. A significant obstacle in developing STAT-3 inhibitors is the demonstration of the antitumor efficacy in in vivo systems and the lack of animal models for human tumors. Therefore, it is crucial to determine whether available STAT-3 inhibitors are suitable for clinical trials. Moreover, further preclinical studies are necessary to focus on the impact of STAT-3 inhibitors on tumor cells. When considering STAT-3 hyper-activation in human cancer, selective targeting to these proteins holds promise for significant advancement in cancer treatment. In the present study, advances in our knowledge of the structure of STAT-3 protein and its regulatory mechanisms are summarized. Moreover, the STAT-3 signaling pathway and its critical role in malignancy are discussed, in addition to the development of STAT-3 inhibitors in various cancer types. Contents 1. Introduction 2. STAT-3 structure 3. STAT-3 signal transduction cascade 4. Target genes regulated by STAT-3 5. Advances in antitumor therapeutics targeting STAT-3 6. Conclusions

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Section: Introductionmentioning

confidence: 99%

Overview of the STAT‑3 signaling pathway in cancer and the development of specific inhibitors (Review)

Mohammad

Liu

2020

Oncol Lett

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“…It was indicated that MAP1LC3A was likeyly to play an indispensable role in the progression of BC. Nowak EM et al [22] revealed that DIRAS3 could regulate cell cycle and impair the growth and movement of cancer cells, all of which might be indirectly dependended on the interaction with STAT3. The down-regulation of DIRAS3 expression was related to the progression of BC, while the restoration of DIRAS3 expression could restain cell proliferation and invasiveness.…”

Section: Discussionmentioning

confidence: 99%

Five crucial prognostic-related autophagy genes stratified female breast cancer patients aged 40-60 years

Zhang

Liu

et al. 2020

Preprint

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Background: Autophagy is closely related to the progression of breast cancer.The aim of this study is to establish a prognostic-related model comprised of hub autophagy-genes(AGs) to assess patitents prognosis. Simultaneously, the model can guide clinicians to make up individualized strategies and stratify patients aged 40-60 years based on risk level.Methods: The hub AGs were identified through univariate COX regression and LASSO regression. The functions and alterations of these selected AGs were analyzed as well.Moreover,the multivariate COX regression and correlation analysis between hub AGs and clinicopathological parameters were done. Results: Totally,33 prognostic-related AGs were obtained from the univariate COX regression(P<0.05).SERPINA1, HSPA8, HSPB8, MAP1LC3A, and DIRAS3 were identified to constitute the prognostic model by the LASSO regression. The survival curve of patients in high-risk and in low-risk group was statistically significant(P<0.05).The 3-year and 5-year ROC displayed that their AUC value reached 0.762 and 0.825,respectively. Stage and riskscore were independent risk factors relevant about prognosis.RB1CC1, RPS6KB1, and BIRC6 were identified as the most predominant mutant genes. It was found that AGs were mainly involved in regulating the endopeptidases synthesis and played important roles in ErbB signal pathway. SERPIN1, riskscore were closely related to stage(P<0.05); HSPA8, riskscore were closely related to T staging(P<0.05); HSPB8 was closely related to N staging(P<0.05). Conclusions: Our prognostic model had relatively robust predictive ability on prognosis for patients aged 40-60 years.If stage was added into the prognostic model, the predictive ability would be more powerful.

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“…In many cases, TAM-derived IL-6 and other cytokines activate STAT3 to promote tumor development by inducing proliferation and inhibiting apoptosis [ 26 ]. Many new drugs, such as DNA methyltransferase inhibitors, can promote tumor cell apoptosis, cell proliferation, angiogenesis, and distant metastasis by inhibiting the phosphorylation of STAT3 [ 27 – 30 ]. In addition, studies have shown that activated STAT3 (p-STAT3) can induce the expression of VEGF [ 31 , 32 ].…”

Section: Discussionmentioning

confidence: 99%

In Vitro and In Vivo Inhibitory Effect of Gujin Xiaoliu Tang in Non‐Small Cell Lung Cancer

Hou

Zhou

et al. 2018

Evidence-Based Complementary and Alternative Medicine

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Non-small cell lung cancer (NSCLC) is a serious threat to people's health. This study aims to determine the possible effect of Gujin Xiaoliu Tang (GJXLT) on NSCLC, which is an empirical formula from Professor Dai-Han Zhou. In this study, chromatographic fingerprinting of GJXLT and A549 cell model in vitro and in vivo was established. We cultured A549 cells in vitro and found that GJXLT inhibited A549 cell growth and induced apoptosis. Compared with the control group, the expression of p-STAT3 and VEGF proteins in the GJXLT groups was decreased. Similar findings were also observed in vivo. First, GJXLT inhibited the growth of transplanted tumor and did not reduce the weight of the tumor-bearing mice in comparison with that of the control group. Then, the Ki-67 expression of transplanted tumor in the GJXLT groups was decreased. In addition, the apoptosis rate of transplanted tumor in the GJXLT groups was increased. Overall, our data showed that GJXLT inhibited A549 cell proliferation and induced apoptosis in vivo and in vitro. Furthermore, GJXLT inhibited the growth of lung cancer xenograft in nude mice model with no obvious side effects. The anti-tumor effect of GJXLT might also be related to the inhibition of p-STATS and VEGF expression in the JAK2/STAT3 pathway. Our results demonstrated the potential of GJXLT as a novel treatment for NSCLC.

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DNA methyltransferase inhibitors influence on the DIRAS3 and STAT3 expression and in vitro migration of ovarian and breast cancer cells

Cited by 11 publications

References 25 publications

Overview of the STAT‑3 signaling pathway in cancer and the development of specific inhibitors (Review)

Overview of the STAT‑3 signaling pathway in cancer and the development of specific inhibitors (Review)

Five crucial prognostic-related autophagy genes stratified female breast cancer patients aged 40-60 years

In Vitro and In Vivo Inhibitory Effect of Gujin Xiaoliu Tang in Non‐Small Cell Lung Cancer

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