Increased Signal Transducer and Activator of Transcription 3 (STAT3) and Decreased Cyclin D1 in Recurrent Astrocytic Tumours Compared with Paired Primary Astrocytic Tumours

Zhang, K; Pang, Bo; Xin, Tao; Hou, Xuben; Jia, Jihui; Feng, Bin; Meng, Liangliang; Xu, Shulan; Pang, Qi

doi:10.1177/147323001103900606

Cited by 4 publications

(4 citation statements)

References 31 publications

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“…Aberrant STAT3 activation is associated with radiation resistance in gliomas. Consistently, in patients with a high risk of recurrence after radiotherapy, there was pronounced STAT3 activation in gliomas (Zhang et al, 2011). As previously described, activation of STAT3 requires phosphorylation of its tyrosine (STAT3-Y705) residue and serine 727 (STAT3-S727) residue.…”

Section: Relationship Between Radiotherapy and Stat3supporting

confidence: 80%

Roles of STAT3 in the pathogenesis and treatment of glioblastoma

Hou²,

Dong³

et al. 2023

Front. Cell Dev. Biol.

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Glioblastoma (GBM) is the most malignant of astrocytomas mainly involving the cerebral hemispheres and the cerebral cortex. It is one of the fatal and refractory solid tumors, with a 5-year survival rate of merely 5% among the adults. IL6/JAK/STAT3 is an important signaling pathway involved in the pathogenesis and progression of GBM. The expression of STAT3 in GBM tissues is substantially higher than that of normal brain cells. The abnormal activation of STAT3 renders the tumor microenvironment of GBM immunosuppression. Besides, blocking the STAT3 pathway can effectively inhibit the growth and metastasis of GBM. On this basis, inhibition of STAT3 may be a new therapeutic approach for GBM, and the combination of STAT3 targeted therapy and conventional therapies may improve the current status of GBM treatment. This review summarized the roles of STAT3 in the pathogenesis of GBM and the feasibility of STAT3 for GBM target therapy.

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Section: Relationship Between Radiotherapy and Stat3supporting

confidence: 80%

Roles of STAT3 in the pathogenesis and treatment of glioblastoma

Hou²,

Dong³

et al. 2023

Front. Cell Dev. Biol.

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“…This suggests an involvement of STAT3 pathway in glioma progression and a possible link with resistance to treatment. This is strengthened by a report showing that recurrent astrocytic glioma displayed an increased STAT3 protein accumulation compared to primary astrocytic tumors [210].…”

Section: Role Of Stat3 Activation In Glioma Resistance To Standard Trmentioning

confidence: 72%

Role of STAT3 in Genesis and Progression of Human Malignant Gliomas

et al. 2016

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Signal transducer and activator of transcription 3 (STAT3) is aberrantly activated in glioblastoma and has been identified as a relevant therapeutic target in this disease and many other human cancers. After two decades of intensive research, there is not yet any approved STAT3-based glioma therapy. In addition to the canonical activation by tyrosine 705 phosphorylation, concordant reports described a potential therapeutic relevance of other post-translational modifications including mainly serine 727 phosphorylation. Such reports reinforce the need to refine the strategy of targeting STAT3 in each concerned disease. This review focuses on the role of serine 727 and tyrosine 705 phosphorylation of STAT3 in glioma. It explores their contribution to glial cell transformation and to the mechanisms that make glioma escape to both immune control and standard treatment.

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“…Similarly, another study demonstrated that the levels of JAK2 and STAT3 are significantly upregulated and exhibit pairwise correlation in human glioma tissues (14). The overexpression of constitutively active STAT3 has also been observed to be accompanied by the restoration of cyclin D1 expression (15); however, there is evidence that increased STAT3 and decreased cyclin D1 protein levels may contribute to the recurrence of astrocytic tumors (16). Therefore, the exact regulation of and relationship between STAT3 and cyclin D1 in glioma remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Annexin�A2 regulates glioma cell proliferation through the STAT3‑cyclin�D1 pathway

et al. 2019

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Annexin A2 (ANXA2) acts as a calcium-dependent phospholipid-binding protein that is widely expressed in vertebrate cells and has abnormally high expression in various tumor cells. However, the detailed molecular mechanism underlying the effects of ANXA2 on glioma cells remains unclear. The present study aimed to investigate the role and underlying molecular mechanisms of ANXA2 in glioma cell proliferation. The results revealed that knockdown of ANXA2 inhibited the proliferation of U251 and U87 glioma cell lines and decreased phosphorylated (p) signal transducer and activator of transcription 3 (STAT3) (Y705) and cyclin D1 expression, leading to impedance of the G 1 -to-S phase transition. Furthermore, it was suggested that ANXA2 may regulate pSTAT3 (Y705) levels through direct binding with STAT3, thereby affecting STAT3-cyclin D1 pathway-mediated cell proliferation. When ANXA2 was re-expressed in ANXA2-knockdown cells, the expression of pSTAT3 (Y705) and cyclin D1 was restored. Furthermore, overexpression of ANXA2 significantly promoted the proliferation of U251 cells, as determined by an MTT assay and a tumor formation assay in nude mice, but had no statistically significant effect on colony formation rate, cell cycle progression or the STAT3-cyclin D1 pathway, suggesting that endogenous ANXA2 may be redundant. Additionally, the present study provided evidence that the overexpression of ANXA2 enhanced the expression of pSTAT3 (Y705) in the presence of epidermal growth factor (EGF), indicating that the proliferation-promoting effect of ANXA2 may be due to the accumulation and synergistic effect of paracrine EGF. Taken together, the present results indicated that ANXA2 may affect the proliferation of human glioma cells through the STAT3-cyclin D1 pathway via direct interaction with STAT3 in U251 and U87 glioma cells. ANXA2 was redundant in this pathway, but positive synergy was revealed to exist between ANXA2 and EGF.

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Increased Signal Transducer and Activator of Transcription 3 (STAT3) and Decreased Cyclin D1 in Recurrent Astrocytic Tumours Compared with Paired Primary Astrocytic Tumours

Cited by 4 publications

References 31 publications

Roles of STAT3 in the pathogenesis and treatment of glioblastoma

Roles of STAT3 in the pathogenesis and treatment of glioblastoma

Role of STAT3 in Genesis and Progression of Human Malignant Gliomas

Annexin�A2 regulates glioma cell proliferation through the STAT3‑cyclin�D1 pathway

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