SYT7 acts as an oncogene and a potential therapeutic target and was regulated by ΔNp63α in HNSCC

Fu, Yuli; Tian, Guocai; Zhang, Zhiyuan; Yang, Xiao

doi:10.1186/s12935-021-02394-w

Cited by 10 publications

(7 citation statements)

References 45 publications

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“…Double knockdown of FBXW7 and circ_RNF13 partially rescued the reduction of TRIM24 and DDX27. Partial rescue effects by double knockdown have also been reported in previous studies [ 33 , 34 ]. Our findings suggest that FBXW7 might not be the only downstream effector of the circ_RNF13/TRIM24/DDX27 axis.…”

Section: Discussionsupporting

confidence: 80%

Circ_RNF13 Regulates the Stemness and Chemosensitivity of Colorectal Cancer by Transcriptional Regulation of DDX27 Mediated by TRIM24 Stabilization

Guo

Tian

et al. 2022

Cancers

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Background: Colorectal cancer (CRC) is one of the most commonly diagnosed cancers with high incidence and poor prognosis worldwide. Circ_RNF13 is upregulated in CRC; however, the biological roles and downstream signaling of circ_RNF13 remain undefined. Methods: The characterization of circ_RNF13 was determined by Sanger sequencing, qRT-PCR, subcellular fractionation assay, and RNA FISH. Western blot analysis and qRT-PCR were employed to detect the expression of the key molecules and stemness markers in CRC tumor samples and cells. The stem-like activities of CRC cells were assessed by sphere formation assay, flow cytometry, and immunofluorescence (IF). Cell viability was monitored by CCK-8 assay. The chemosensitivity of CRC cells was assessed by colony formation and cell apoptosis assays. Bioinformatics analysis, RIP assay, RNA pull-down assay, and FISH/IF staining were used to detect the association between circ_RNF13 and TRIM24. The transcriptional regulation of DDX27 was investigated by ChIP assay, and the post-translational regulation of TRIM24 was detected by Co-IP. The in vitro findings were verified in a xenograft model. Results: circ_RNF13 and DDX27 were elevated in CRC tumor samples and cells. Knockdown of circ_RNF13 or DDX27 inhibited stemness and increased chemosensitivity in CRC cells. Mechanistically, circ_RNF13 regulated DDX27 expression via TRIM24-mediated transcriptional regulation, and circ_RNF13 stabilized TRIM24 via suppressing FBXW7-mediated TRIM24 degradation. In vivo studies revealed that the knockdown of circ_RNF13 impaired stemness and enhanced the chemosensitivity of CRC in the xenograft model. Conclusion: circ_RNF13 regulated the stemness and chemosensitivity of CRC by transcriptional regulation of DDX27 mediated by TRIM24 stabilization.

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Section: Discussionsupporting

confidence: 80%

Circ_RNF13 Regulates the Stemness and Chemosensitivity of Colorectal Cancer by Transcriptional Regulation of DDX27 Mediated by TRIM24 Stabilization

Guo

Tian

et al. 2022

Cancers

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“…Syt7 is significantly upregulated in non-small cell lung cancer, thyroid cancer, and HNSCC [15][16][17]. Increased Syt7 promotes cancer cell proliferation and inhibits cancer cell apoptosis [15][16][17]. Syt7 interacts with BRCA1 to suppress the ubiquitination of HMGB3, which contributes to the role of Syt7 in thyroid cancer [16].…”

Section: Discussionmentioning

confidence: 99%

“…In the autonomic nervous system, Syt7 has been identified expressed in the sympathetic nerve terminals, regulates Ca 2+ ‐dependent norepinephrine (NE) exocytosis and enhances Ca 2+ ‐independent NE overflow [14]. Besides, Syt7 has been demonstrated to mediate several tumorigenesis such as lung cancer [15], thyroid cancer [16], and head and neck squamous cell carcinoma (HNSCC) [17]. Recent advance has revealed that Syt7 participates in vascular diseases.…”

Section: Introductionmentioning

confidence: 99%

Synaptotagmin‐7 mediates cardiac hypertrophy by targeting autophagy

Sun,

Han,

et al. 2023

The FEBS Journal

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Sustained cardiac hypertrophy damages the heart and weakens cardiac function, often leading to heart failure and even death. Pathological cardiac hypertrophy has become a central therapeutic target for many heart diseases including heart failure. However, the underlying mechanisms of cardiac hypertrophy, especially the involvement of autophagy program, are still ill‐understood. Synaptotagmin‐7 (Syt7), a multifunctional and high‐affinity calcium sensor, plays a pivotal role in asynchronous neurotransmitter release, synaptic facilitation and vesicle pool regulation during synaptic transmission. However, little is known about whether Syt7 is expressed in the myocardium and involved in the pathogenesis of heart diseases. Here we showed that Syt7 was significantly upregulated in Ang II‐treated hearts and cardiomyocytes. Homozygous syt7 knockout (syt7‐/‐) mice exhibited significantly attenuated cardiac hypertrophy and fibrosis and improved cardiac function. We further found that Syt7 exerted a pro‐hypertrophic effect by suppressing the autophagy process. In exploring the upstream mechanisms, microRNA (miR)‐93 was identified to participate in the regulation of Syt7 expression. MiR‐93 protected hearts against Ang II‐induced hypertrophy through targeting Syt7‐autophagy pathway. In summary, our data reveal a new cardiac hypertrophy regulator and a novel hypertrophy regulating model composed of miR‐93, Syt7 and autophagy program. These molecules may serve as potential therapeutic targets in the treatment of cardiac hypertrophy and heart failure.

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“…They also found that ΔNp63α could affect HNSCC cells by downregulating the expression of SYT7 in vitro , including inhibiting proliferation, promoting apoptosis, and reducing the proportion of cancer cells in G1 phase. Therefore, the ΔNp63α/SYT7 axis might be a potential clinically effective target for the treatment of HNSCC ( 29 ).…”

Section: Roles Of Synaptotagmin Family Members In Cancersmentioning

confidence: 99%

Potential roles of synaptotagmin family members in cancers: Recent advances and prospects

2022

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With the continuous development of bioinformatics and public database, more and more genes that play a role in cancers have been discovered. Synaptotagmins (SYTs) are abundant, evolutionarily conserved integral membrane proteins composed of a short N-terminus, a variable linker domain, a single transmembrane domain, and two C2 domains, and they constitute a family of 17 isoforms. The synaptotagmin family members are known to regulate calcium-dependent membrane fusion events. Some SYTs play roles in hormone secretion or neurotransmitter release or both, and much evidence supports SYTs as Ca2+ sensors of exocytosis. Since 5 years ago, an increasing number of studies have found that SYTs also played important roles in the occurrence and development of lung cancer, gastric cancer, colon cancer, and other cancers. Down-regulation of SYTs inhibited cell proliferation, migration, and invasion of cancer cells, but promoted cell apoptosis. Growth of peritoneal nodules is inhibited and survival is prolonged in mice administrated with siSYTs intraperitoneally. Therefore, most studies have found SYTs serve as an oncogene after overexpression and may become potential prognostic biomarkers for multiple cancers. This article provides an overview of recent studies that focus on SYT family members’ roles in cancers and highlights the advances that have been achieved.

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SYT7 acts as an oncogene and a potential therapeutic target and was regulated by ΔNp63α in HNSCC

Cited by 10 publications

References 45 publications

Circ_RNF13 Regulates the Stemness and Chemosensitivity of Colorectal Cancer by Transcriptional Regulation of DDX27 Mediated by TRIM24 Stabilization

Circ_RNF13 Regulates the Stemness and Chemosensitivity of Colorectal Cancer by Transcriptional Regulation of DDX27 Mediated by TRIM24 Stabilization

Synaptotagmin‐7 mediates cardiac hypertrophy by targeting autophagy

Potential roles of synaptotagmin family members in cancers: Recent advances and prospects

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