RETRACTED ARTICLE: MicroRNA-572/hMOF/Sirt6 regulates the progression of ovarian cancer

Cai, Mingbo; Hu, Zhenhua; Liang, Han; Guo, Ruixia

doi:10.1080/15384101.2020.1809258

Cited by 3 publications

(3 citation statements)

References 37 publications

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“…PC has been demonstrated to rely on cysteine metabolism to prevent ferroptosis induced by ROS ( 35 ). SIRT6 could inhibit the growth of various malignant tumors ( 26 , 36 , 37 ). SIRT6 and SIRT6-mediated restraining of SIRT1 could induce head and neck cancers cell death by enhancing the level of intracellular ROS ( 38 ).…”

Section: Discussionmentioning

confidence: 99%

SIRT6 promotes ferroptosis and attenuates glycolysis in pancreatic cancer through regulation of the NF‑κB pathway

et al. 2022

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Pancreatic cancer (PC) is a malignant tumor with high mortality worldwide. SIRT6 plays versatile roles in human cancers. However, SIRT6 has rarely been studied in PC. The purpose of the present study was to explore the function and potential mechanism of SIRT6 in PC. The expression of SIRT6 in PC tissues and cells was detected by reverse transcription-quantitative PCR and western blotting. The overall survival time was analyzed through the Kaplan Meier method. Cell viability was measured by the Cell Counting Kit-8 assay. The Fe 2+ content, glucose uptake, lactic acid and ATP production were detected through the corresponding kits. ROS was evaluated using the DCFH-DA detection kit. Protein expression was assessed by immunohistochemistry or western blot analysis. In the present study, SIRT6 was lowly expressed in PC tissues and cells compared with normal tissues and cells. Moreover, the low expression of SIRT6 was associated with a poor prognosis in patients with PC. Upregulation of SIRT6 significantly promoted the ferroptosis and inhibited the glycolysis in PC cells. However, knockdown of SIRT6 resisted ferroptosis and increased glycolysis in PC cells. Further studies found that the activation of NF-κB could reverse the effect of SIRT6 on PC cells. In addition, overexpression of SIRT6 restrained the growth of xenografted tumors and suppressed the nuclear transcription of NF-κB in vivo . Collectively, the present study indicated that SIRT6 promoted ferroptosis and inhibited glycolysis through inactivating the NF-κB signaling pathway in PC. These findings suggested that SIRT6 may become a therapeutic target for PC.

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Section: Discussionmentioning

confidence: 99%

SIRT6 promotes ferroptosis and attenuates glycolysis in pancreatic cancer through regulation of the NF‑κB pathway

et al. 2022

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“…Another study reported that MOF was significantly upregulated at the protein level in hepatocellular carcinoma with microvascular invasion, and MOF downregulation would reduce the intravasation and metastasis in vitro and in vivo ( 26 ). On the contrary, the mRNA and protein levels of MOF were abnormally down-regulated in ovarian cancer tissues and cells, and the overexpression of MOF could inhibit the growth of ovarian cancer cells and promote cell apoptosis ( 27 ). Moreover, MOF-mediated H4K16Ac could promote the release of RNA polymerase II from pausing through recruiting BRD4 and pTEFb, and lead to reactivation of tumor suppressor TMS1 ( 16 ).…”

Section: Discussionmentioning

confidence: 99%

The Histone Acetyltransferase MOF Regulates SIRT1 Expression to Suppress Renal Cell Carcinoma Progression

et al. 2022

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BackgroundRenal cell carcinoma (RCC) is one of the most common and lethal human urological malignancies around the world. Although many advancements in diagnostic and therapeutic strategies have been acquired, the prognosis of patients with metastatic RCC was poor. Thus, there is an urgent need to understand the molecular mechanism of RCC.MethodsThe quantitative real-time PCR (qRT-PCR) was used to detect the RNA expression of MOF in human RCC tissues and cell lines. The protein expression of MOF was analyzed with immunohistochemistry (IHC) and Western blot. To understand the regulatory mechanism of MOF in liver cancer, ChIP-qPCR assay and dual-luciferase assay were performed. Moreover, a series of in vivo and in vitro experiments were conducted to evaluate the effect of MOF on renal cell carcinoma progression.ResultsIn the present study, we found that Males absent on the first (MOF), a histone acetyltransferase involved in transcription activation, was significantly decreased in both RCC tissues and RCC cells compared to normal tissues and non-cancer cells. Moreover, MOF downregulation was associated with advanced histological grade, pathologic stage and distant metastasis of RCC patients. Ectopic expression of MOF could significantly attenuate cell proliferation and promote cell apoptosis. Besides, MOF overexpression also suppressed migration of RCC cells through inhibiting epithelial-mesenchymal transition (EMT). Importantly, the inhibition of tumor growth by MOF was further confirmed by in vivo studies. Mechanism dissection revealed that MOF could transcriptionally upregulate the expression of SIRT1, leading to attenuated STAT3 signaling, which was involved in cell proliferation and migration. Moreover, SIRT1 knockdown could restore the biological function induced by MOF overexpression.ConclusionsOur findings indicated that MOF serves as a tumor suppressor via regulation of SIRT1 in the development and progression of RCC, and MOF might be a potent biomarker for diagnosis and prognosis prediction of RCC patients.

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“…Besides, several research studies have reported that SIRT6 plays an important role in DNA damage, repair, and mutagenesis [12,13]. In recent years, more and more studies have reported the distinct dysregulation of SIRT6 in many types of tumors [14,15]. However, the expressing pattern of SIRT6 exhibited a different trend based on the types of tumors.…”

Section: Introductionmentioning

confidence: 99%

SIRT6 Promotes the Progression of Prostate Cancer via Regulating the Wnt/β-Catenin Signaling Pathway

Zhang

Chen

Song

et al. 2022

Journal of Oncology

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Sirtuin 6 (SIRT6), a DNA repair-related gene, has undergone an extremely thorough study for its involvement in the development of many different cancers. The objective of our study was to explore the function and mechanism of SIRT6-induced regulation of prostate cancer (PCa). RT-PCR was performed to validate the levels of SIRT6 in PCa cell lines. Cell proliferation, migration, and invasion of cells with SIRT6 knockdown were assessed using CCK-8 assay, colony formation assay, wound-healing assay, and transwell assay. Western blot was applied to assess the related proteins. We found that SIRT6 expression was distinctly upregulated in PCa specimens and cells. Loss-of-functional assays revealed that SIRT6 silence suppressed the proliferation and metastasis of PCa cells. Mechanistic studies revealed that SIRT6 silence inhibited Wnt/β‐catenin signaling and EMT progress. Overall, the study confirmed the upregulation of SIRT6 in patients with PCa and its association with the progression. SIRT6 promoted PCa progression by regulating Wnt/β‐catenin signaling, providing a promising biomarker and treatment approach for preventing PCa.

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RETRACTED ARTICLE: MicroRNA-572/hMOF/Sirt6 regulates the progression of ovarian cancer

Cited by 3 publications

References 37 publications

SIRT6 promotes ferroptosis and attenuates glycolysis in pancreatic cancer through regulation of the NF‑κB pathway

SIRT6 promotes ferroptosis and attenuates glycolysis in pancreatic cancer through regulation of the NF‑κB pathway

The Histone Acetyltransferase MOF Regulates SIRT1 Expression to Suppress Renal Cell Carcinoma Progression

SIRT6 Promotes the Progression of Prostate Cancer via Regulating the Wnt/β-Catenin Signaling Pathway

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