Adenovirus encoding Smad4 suppresses glioma cell proliferation and increases apoptosis through cell cycle arrest at G1 phase

Yang, Zhao; Zhong, Lina; Zhong, Shanchuan; Xian, Ronghua; Yuan, Bangqing

doi:10.1016/j.intimp.2015.01.022

Cited by 5 publications

(7 citation statements)

References 26 publications

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“…Phosphorylated Smad 2 and Smad 3 form heteromeric complexes with Smad 4 and translocate into the nucleus to regulate cancer‐related genes 13,14 . It is recognized that Smad 4 plays an inhibitory role in tumors, such as breast cancer and glioma 26–29 . In CC cells, TGFβ has the effect of inhibiting cell proliferation and promoting apoptosis 30,31 .…”

Section: Discussionmentioning

confidence: 99%

“…recognized that Smad 4 plays an inhibitory role in tumors, such as breast cancer and glioma. [26][27][28][29] In CC cells, TGFβ has the effect of inhibiting cell proliferation and promoting apoptosis. 30,31 Studies have found that TGFβ exerts a tumor suppressive effect in the early stage of tumors, but in the later stages, its tumor suppressing effect disappears, and it even plays a tumor promoting role.…”

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confidence: 99%

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MiR‐362 suppresses cervical cancer progression via directly targeting BAP31 and activating TGFβ/Smad pathway

et al. 2020

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BAP31 (B‐cell receptor‐associated protein 31) is an important regulator of intracellular signal transduction and highly expressed in several cancer tissues or testicular tissues. Our previous study had revealed that elevated BAP31 plays a crucial role in the progress and metastasis of cervical cancer. Even so, the precise mechanism of abnormal BAP31 elevation in cervical cancer has not been fully elucidated. We revealed that the expression of BAP31 was mainly regulated by microRNA‐362 (miR‐362), which was markedly downregulated in cervical cancer tissues and negatively correlated with clinical tumor staging. Overexpression of miR‐362 inhibited cervical cancer cell proliferation and increased the proportion of apoptotic cells. Furthermore, miR‐362 reduced the tumor sizes and prolonged mice survival time in xenograft nude mice model. Finally, we demonstrated that the BAP31/SPTBN1 complex regulated tumor progression through the Smad 2/3 pathway under the control of miR‐362. Collectively, our findings demonstrated that miR‐362 could work as an anti‐oncomiR that inhibits proliferation and promotes apoptosis in cervical cancer cells via BAP31 and TGFβ/Smad pathway. Overexpression of miR‐362 might be a potential therapeutic strategy for cervical cancer.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

MiR‐362 suppresses cervical cancer progression via directly targeting BAP31 and activating TGFβ/Smad pathway

et al. 2020

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“…These results indicated that the downregulation of Smad4 may cause decreased c-Myc protein expression following the ectopic overexpression of miR-124 in C6 cells. Controversially, other researchers have presented data showing that an adenovirus encoding Smad4 suppresses glioma cell proliferation (39). Therefore, if Smad4 directly controls c-Myc expression in glioma cells, the associated mechanisms should be investigated in greater detail.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-124 inhibits the proliferation of C6 glioma cells by targeting Smad4

Zhang

Gong

et al. 2017

International Journal of Molecular Medicine

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MicroRNA-124 (miR-124) has been shown to be downregulated in glioma; however, its biological functions in glioma are not yet fully understood. The aim of this study was to examine the Smad4‑dependent effects of miR‑124 on C6 glioma cell proliferation. In this study, the level of miR‑124 was found to be enhanced in C6 cells upon transfection with miR‑124 mimics, and the mechanisms of action of miR‑124 in C6 cells were investigated by reverse transcriptase-quantitative polymerase chain reaction, MTT assay, western blot analysis and luciferase reporter assays in vitro. The results revealed that miR‑124 expression was significantly lower in the C6 cells than in either normal rat brain tissue or astrocytes. Upon the overexpression of miR‑124, the proliferation of the C6 cells decreased and Smad4 expression was significantly suppressed. Smad4 was identified as a direct target of miR‑124 through luciferase reporter assays. Furthermore, miR‑124 was found to modulate signal transducer and activator of transcription 3 (Stat3) by downregulating Smad4 expression. Using small interfering RNA targeting Smad4 mRNA, we also confirmed that miR‑124 downregulated c‑Myc by modulating Smad4 expression. In addition, caspase‑3 expression was induced by miR‑124 overexpression, but not via Smad4 downregulation. On the whole, our results demonstrate that miR‑124 upregulation inhibits the growth of C6 glioma cells by targeting Smad4 directly. These findings may be clinically useful for the development of therapeutic strategies directed toward miR‑124 function in patients with glioma.

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“…The Smad4 expression is deregulated in several types of cancers 47 . The overexpression of Smad4 increases apoptosis and suppresses cell proliferation 48 . Smad4 is one of the key signal transducers of TGF-β which regulates cell function and pancreatic cancer development.…”

Section: Roles Of Smad4 In Cancermentioning

confidence: 99%

“…The important point is the boundary between exon 3 and four 82 . A portion of exon 7 and exon 6 adjacent to the MH2 domain (275-322 amino acids) is required for transcription 48 , 81 . The isoforms having deleted exon (∆4-7) is almost lacking the entire linker region is found in papillary thyroid carcinoma.…”

Section: Roles Of Smad4 In Cancermentioning

confidence: 99%

Roles of Smads Family and Alternative Splicing Variants of Smad4 in Different Cancers

Ullah¹,

Sun²,

Tang³

et al. 2018

J. Cancer

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Transforming Growth Factor β (TGF-β) is one of the most common secretory proteins which are recognized by membrane receptors joined to transcription regulatory factor. TGF-β signals are transduced by the Smads family that regulate differentiation, proliferation, early growth, apoptosis, homeostasis, and tumor development. Functional study of TGF-β signaling pathway and Smads role is vital for certain diseases such as cancer. Alternative splicing produces a diverse range of protein isoforms with unique function and the ability to react differently with various pharmaceutical products. This review organizes to describe the general study of Smads family, the process of alternative splicing, the general aspect of alternative splicing of Smad4 in cancer and the possible use of spliceoforms for the diagnosis and therapeutic purpose. The main aim and objective of this article are to highlight some particular mechanisms involving in alternatives splicing of cancer and also to demonstrate new evidence about alternative splicing in different steps given cancer initiation and progression.

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Adenovirus encoding Smad4 suppresses glioma cell proliferation and increases apoptosis through cell cycle arrest at G1 phase

Cited by 5 publications

References 26 publications

MiR‐362 suppresses cervical cancer progression via directly targeting BAP31 and activating TGFβ/Smad pathway

MiR‐362 suppresses cervical cancer progression via directly targeting BAP31 and activating TGFβ/Smad pathway

MicroRNA-124 inhibits the proliferation of C6 glioma cells by targeting Smad4

Roles of Smads Family and Alternative Splicing Variants of Smad4 in Different Cancers

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