SIRT7 Exhibits Oncogenic Potential in Human Ovarian Cancer Cells

Wang, Hong Ling; Lu, Ren Quan; Xie, Su Hong; Zheng, Hui; Wen, Xue Mei; Gao, Xiang; Guo, Lin

doi:10.7314/apjcp.2015.16.8.3573

Cited by 55 publications

(38 citation statements)

References 20 publications

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“…Previous studies have also supported our conclusion, reporting that SIRT7 depletion suppresses apoptosis in various kinds of cells. [27][28][29] Overall, these results are the first to reveal the exosome-mediated therapeutic effect of hUMSCs.…”

Section: Discussionmentioning

confidence: 64%

Exosomal miRNA-17-5p derived from human umbilical cord mesenchymal stem cells improves ovarian function in premature ovarian insufficiency by regulating SIRT7

et al. 2020

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Premature ovarian insufficiency (POI) is clinically irreversible in women aged over 40 years. Although numerous studies have demonstrated satisfactory outcomes of mesenchymal stem cell therapy, the underlying therapeutic mechanism remains unclear. Exosomes were collected from the culture medium of human umbilical cord mesenchymal stem cells (hUMSCs) and assessed by electron microscopy and Western blot (WB) analysis. Then, exosomes were added to the culture medium of cyclophosphamide (CTX)‐damaged human granulosa cells (hGCs), and the mixture was injected into the ovaries of CTX‐induced POI model mice before detection of antiapoptotic and apoptotic gene expression. Next, the microRNA expression profiles of hUMSC‐derived exosomes (hUMSC‐Exos) were detected by small RNA sequencing. The ameliorative effect of exosomal microRNA‐17‐5P (miR‐17‐5P) was demonstrated by miR‐17‐5P knockdown before assessment of ovarian phenotype and function, reactive oxygen species (ROS) levels and SIRT7 expression. Finally, SIRT7 was inhibited or overexpressed by RNA interference or retrovirus transduction, and the protein expression of PARP1, γH2AX, and XRCC6 was analyzed. The ameliorative effect of hUMSC‐Exos on POI was validated. Our results illustrated that hUMSC‐Exos restored ovarian phenotype and function in a POI mouse model, promoted proliferation of CTX‐damaged hGCs and ovarian cells, and alleviated ROS accumulation by delivering exosomal miR‐17‐5P and inhibiting SIRT7 expression. Moreover, our findings elucidated that miR‐17‐5P repressed PARP1, γH2AX, and XRCC6 by inhibiting SIRT7. Our findings suggest a critical role for exosomal miR‐17‐5P and its downstream target mRNA SIRT7 in hUMSC transplantation therapy. This study indicates the promise of exosome‐based therapy for POI treatment.

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Section: Discussionmentioning

confidence: 64%

Exosomal miRNA-17-5p derived from human umbilical cord mesenchymal stem cells improves ovarian function in premature ovarian insufficiency by regulating SIRT7

et al. 2020

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“…Increasing evidence indicates SIRT7 as an oncogene in various types of cancer (34). SIRT7 is overexpressed in hepatocellular carcinoma, cervical, ovarian, colorectal, gastric and lung cancer, and is involved in regulating cancer cell proliferation, apoptosis and metastasis (25,33,39,(47)(48)(49). Ashraf et al (35) demonstrated that SIRT7 was significantly increased in breast cancer associated with node-positive breast cancer.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-3666 inhibits breast cancer cell proliferation by targeting sirtuin 7

2017

Molecular Medicine Reports

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The abnormal expression of microRNAs (miRNAs) is associated with cancer initiation and progression. miRNAs functioning as oncogenes or tumor suppressors represent novel biomarkers for cancer diagnosis, prognosis, and serve as therapeutic tools. MiR‑3666 has been reported as a tumor suppressor in various types of cancer; however, its role in breast cancer remains unknown. In the current study, the aim was to investigate the potential role of miR‑3666 in breast cancer. It was identified that miR‑3666 was decreased in breast cancer cell lines and that the overexpression of miR‑3666 inhibited breast cancer cell proliferation. Furthermore, miR‑3666 promotes cell apoptosis of breast cancer cells. Bioinformatics analysis and dual‑luciferase reporter assay demonstrated that miR‑3666 targeted the 3'‑untranslated region of sirtuin 7 (SIRT7) which was recognized as an oncogene. Overexpression of miR‑3666 decreased SIRT7 expression levels, and knockdown of SIRT7 suppressed proliferation and promoted apoptosis of breast cancer cells. A rescue assay demonstrated that the restoration of SIRT7 expression markedly reversed the miR‑3666‑induced anti‑tumor effects. Thus, the current study indicates that miR‑3666 suppresses breast cancer cell proliferation by targeting SIRT7, and propose miR‑3666 as a potential candidate for breast cancer therapy.

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“…SIRT7 knockdown also inhibits gastric cancer cell growth in vitro and in vivo (34). In addition, SIRT7 is highly expressed in ovarian cancer cell lines, and its loss reduces cell growth and colony formation and promotes cell apoptosis of ovarian cancer cells (35). High SIRT7 expression is also found in breast cancer and is correlated with high histological grade and poor survival rate (36,37).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-3666-induced suppression of SIRT7 inhibits the growth of non-small cell lung cancer cells

Shi

Ji²,

Zhang

et al. 2016

Oncology Reports

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Sirtuin7 (SIRT7) plays an important role in many cancer types, but its function in non-small cell lung cancer (NSCLC) remains unclear. This study investigated the biological role and underlying mechanism of SIRT7 in NSCLC. Results showed that SIRT7 was highly expressed in NSCLC cell lines, as detected by real-time quantitative polymerase chain reaction and western blot analysis. SIRT7 knockdown by small interfering RNA (siRNA) significantly inhibited the growth of NSCLC cells and induced their apoptosis. Bioinformatics algorithms indicated that SIRT7 was a putative target of microRNA-3666 (miR-3666). Dual-luciferase reporter assay demonstrated that miR-3666 could target the 3'-untranslated region of SIRT7. Western blot analysis revealed that miR-3666 could regulate the protein expression of SIRT7. The miR-3666 overexpression significantly inhibited NSCLC cell growth. The restoration of SIRT7 protein expression significantly abrogated the effect of the miR-3666 overexpression. Moreover, SIRT7 depletion induced by siRNA or miR-3666 overexpression promoted the expression of pro-apoptotic genes. Taken together, our study suggests that SIRT7 functions as an oncogene in NSCLC, and miR-3666 can target SIRT7 to inhibit NSCLC cell growth by promoting the pro-apoptotic signaling pathway. Thus, this study provides novel insights into the development of new and potential treatments for NSCLC.

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SIRT7 Exhibits Oncogenic Potential in Human Ovarian Cancer Cells

Cited by 55 publications

References 20 publications

Exosomal miRNA-17-5p derived from human umbilical cord mesenchymal stem cells improves ovarian function in premature ovarian insufficiency by regulating SIRT7

Exosomal miRNA-17-5p derived from human umbilical cord mesenchymal stem cells improves ovarian function in premature ovarian insufficiency by regulating SIRT7

MicroRNA-3666 inhibits breast cancer cell proliferation by targeting sirtuin 7

MicroRNA-3666-induced suppression of SIRT7 inhibits the growth of non-small cell lung cancer cells

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