SOX30, a target gene of miR-653-5p, represses the proliferation and invasion of prostate cancer cells through inhibition of Wnt/β-catenin signaling

Fu, Qiang; Sun, Zhen; Yang, Fan; Mao, Tianci; Gao, Yanyao; Wang, He

doi:10.1186/s11658-019-0195-4

Cited by 33 publications

(30 citation statements)

References 42 publications

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“…It has recently been identi ed as a cancer-related miRNA for several cancers. For example, Fu et al declared that miR-653-5p was highly expressed in prostate cancer tissues, and miR-653-5p knockdown limited prostate cancer cell proliferation and metastasis via inhibiting Wnt/β-catenin signaling [37]. Han, et al proved that miR-653-5p acted as a tumor-suppressive miRNA through targeting TIAM1 to suppress lung cancer cell proliferation and invasion [38].…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA XIST suppresses tumorigenesis and enhances radiosensitivity in neuroblastoma cells through regulating miR-653-5p/HK2 axis

Mou

Wang

Zhang

et al. 2020

Preprint

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Background: Abnormal expression of long noncoding RNAs (lncRNAs) was usually involved in tumorigenesis and radiosensitivity of various cancers. The aim of this study was to explore the biological function and regulatory mechanism of lncRNA X-inactive specific transcript (XIST) in tumorigenesis and radiosensitivity of neuroblastoma (NB).Methods: The expression levels of XIST, microRNA-653-5p (miR-653-5p) and hexokinase 2 (HK2) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Methylthiazolyldiphenyl tetrazolium bromide (MTT) assay, colony formation assay and transwell assay were utilized to detect cell viability, colony formation and cell invasion abilities. Glucose consumption or lactate production was measured by glucose assay kit or lactate assay kit, respectively. The mice xenograft model was established to investigate the role of XIST in vivo. The interaction between miR-653-5p and XIST or HK2 was predicted by starBase v2.0 and verified by dual-luciferase reporter, RNA Immunoprecipitation (RIP) and RNA pull-down assays. Western blot was used to measure the protein expression of HK2.Results: XIST and HK2 were highly expressed whilst miR-653-5p was lowly expressed in NB tissues and cells. XIST knockdown inhibited tumorigenesis by repressing NB cell proliferation and invasion. Meanwhile, XIST downregulation increased the radiosensitivity via inhibiting colony formation rates and glycolysis. Moreover, miR-653-5p could bind to XIST and its downregulation reversed the effects of XIST knockdown on tumorigenesis and radiosensitivity. Additionally, HK2 was a direct target of miR-653-5p and its overexpression attenuated the effects of miR-653-5p restoration on suppression of tumorigenesis and promotion of radiosensitivity. Besides, XIST functioned as a molecular sponge of miR-653-5p to regulate HK2 expression. Furthermore, XIST knockdown also suppressed tumor growth by upregulating miR-653-5p and downregulating HK2 in vivo.Conclusion: XIST interference inhibited tumorigenesis and increased radiosensitivity in NB by regulating miR-653-5p/HK2 axis, providing a novel therapeutic strategy for NB.

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Section: Discussionmentioning

confidence: 99%

Long noncoding RNA XIST suppresses tumorigenesis and enhances radiosensitivity in neuroblastoma cells through regulating miR-653-5p/HK2 axis

Mou

Wang

Zhang

et al. 2020

Preprint

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“…It has recently been identified as a cancer-related miRNA for several cancers. For example, Fu et al declared that miR-653-5p was highly expressed in prostate cancer tissues, and miR-653-5p knockdown limited prostate cancer cell proliferation and metastasis via inhibiting Wnt/β-catenin signaling [33]. Han, et al proved that miR-653-5p acted as a tumor-suppressive miRNA through targeting TIAM1 to suppress lung cancer cell proliferation and invasion [34].…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA XIST suppresses tumorigenesis and enhances radiosensitivity in neuroblastoma cells through regulating miR-653-5p/HK2 axis

Wang

Zhang

et al. 2020

Preprint

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Background: Abnormal expression of long noncoding RNAs (lncRNAs) was usually involved in tumorigenesis and radiosensitivity of various cancers. The aim of this study was to explore the biological function and regulatory mechanism of lncRNA X-inactive specific transcript (XIST) in tumorigenesis and radiosensitivity of neuroblastoma (NB).Methods: The expression levels of XIST, microRNA-653-5p (miR-653-5p) and hexokinase 2 (HK2) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Methylthiazolyldiphenyl tetrazolium bromide (MTT) assay, colony formation assay and transwell assay were utilized to detect cell viability, colony formation and cell invasion abilities. Glucose consumption or lactate production was measured by glucose assay kit or lactate assay kit, respectively. The mice xenograft model was established to investigate the role of XIST in vivo. The interaction between miR-653-5p and XIST or HK2 was predicted by starBase v2.0 and verified by dual-luciferase reporter assay. Western blot was used to measure the protein expression of HK2.Results: XIST and HK2 were highly expressed whilst miR-653-5p was lowly expressed in NB tissues and cells. XIST knockdown inhibited tumorigenesis by repressing NB cell proliferation and invasion. Meanwhile, XIST downregulation increased the radiosensitivity via inhibiting colony formation rates and glycolysis. Moreover, miR-653-5p could bind to XIST and its downregulation reversed the effects of XIST knockdown on tumorigenesis and radiosensitivity. Additionally, HK2 was a direct target of miR-653-5p and its overexpression attenuated the effects of miR-653-5p restoration on suppression of tumorigenesis and promotion of radiosensitivity. Besides, XIST functioned as a molecular sponge of miR-653-5p to regulate HK2 expression. Furthermore, XIST knockdown also suppressed tumor growth by upregulating miR-653-5p and downregulating HK2 in vivo.Conclusion: XIST interference inhibited tumorigenesis and increased radiosensitivity in NB by regulating miR-653-5p/HK2 axis, providing a novel therapeutic strategy for NB.

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“…The potential role of the SOX30 protein in prostate, bladder and colon cancers has also been studied [179][180][181]. In prostate cancer, SOX30 acts as a tumor suppressor, similarly to what happens in other types of cancer.…”

Section: Sox30mentioning

confidence: 99%

“…Moreover, it was discovered that a lower SOX30 expression in Prostate Cancer (PC) cells compared to normal tissue cells is caused by the inhibiting effect of miR-653-5p's interaction with the SOX30 transcript, which results in the downregulation of Wnt/β-catenin signaling. This miR-653-5p/SOX30/Wnt/β-catenin axis may be involved in the progression of prostate cancer [179]. The overexpression of SOX30 reduces Wnt/β-catenin signaling, therefore targeting SOX30 in PC patients could be a promising choice for innovative anticancer therapy.…”

Section: Sox30mentioning

confidence: 99%

Role of SOX Protein Groups F and H in Lung Cancer Progression

Olbromski¹,

Podhorska‐Okołów

Dzięgiel

2020

Cancers

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The SOX family proteins are proved to play a crucial role in the development of the lymphatic ducts and the cardiovascular system. Moreover, an increased expression level of the SOX18 protein has been found in many malignances, such as melanoma, stomach, pancreatic breast and lung cancers. Another SOX family protein, the SOX30 transcription factor, is responsible for the development of male germ cells. Additionally, recent studies have shown its proapoptotic character in non-small cell lung cancer cells. Our preliminary studies showed a disparity in the amount of mRNA of the SOX18 gene relative to the amount of protein. This is why our attention has been focused on microRNA (miRNA) molecules, which could regulate the SOX18 gene transcript level. Recent data point to the fact that, in practically all types of cancer, hundreds of genes exhibit an abnormal methylation, covering around 5–10% of the thousands of CpG islands present in the promoter sequences, which in normal cells should not be methylated from the moment the embryo finishes its development. It has been demonstrated that in non-small-cell lung cancer (NSCLC) cases there is a large heterogeneity of the methylation process. The role of the SOX18 and SOX30 expression in non-small-cell lung cancers (NSCLCs) is not yet fully understood. However, if we take into account previous reports, these proteins may be important factors in the development and progression of these malignancies.

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SOX30, a target gene of miR-653-5p, represses the proliferation and invasion of prostate cancer cells through inhibition of Wnt/β-catenin signaling

Cited by 33 publications

References 42 publications

Long noncoding RNA XIST suppresses tumorigenesis and enhances radiosensitivity in neuroblastoma cells through regulating miR-653-5p/HK2 axis

Long noncoding RNA XIST suppresses tumorigenesis and enhances radiosensitivity in neuroblastoma cells through regulating miR-653-5p/HK2 axis

Long noncoding RNA XIST suppresses tumorigenesis and enhances radiosensitivity in neuroblastoma cells through regulating miR-653-5p/HK2 axis

Role of SOX Protein Groups F and H in Lung Cancer Progression

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