lncRNA SNHG15 Promotes Ovarian Cancer Progression through Regulated CDK6 via Sponging miR-370-3p

Wang, Yi; Ding, Minghong; Yuan, Xiaoqing; Ruibao, Jiao; Zhu, Dagao; Huang, Wanzhong; Deng, Wenxia; Liu, Yulong

doi:10.1155/2021/9394563

Cited by 9 publications

(10 citation statements)

References 30 publications

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“…A previous study has revealed that miR-204 suppresses nonsmall cell lung cancer (NSCLC) progression through downregulating the CDK6 level [ 28 ]. Similarly, a recent study has indicated that miR-370-3p restrains the progression of ovarian cancer by reducing CDK6 expression [ 29 ]. Moreover, miR-576 represses CDK6 expression to promote bladder cancer cell proliferation [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

FOXO1-Induced miR-502-3p Suppresses Colorectal Cancer Cell Growth through Targeting CDK6

Fan

Zhao

et al. 2023

Journal of Oncology

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Colorectal cancer (CRC) is the most common tumor of the digestive system and the third most common tumor worldwide. To date, the prognosis of CRC patients remains poor. It is urgent to identify new therapeutic targets for CRC. As a tumor suppresser, microRNA (miRNA) miR-502-5p is downregulated in CRC tissues. Nevertheless, the role of miR-502-3p in CRC is largely unclear. Besides, the transcript factor forkhead box protein O1 (FOXO1) could suppress the CRC cell growth. However, the effect of FOXO1 on miR-502-3p in CRC remains unknown. By contrast, cyclin-dependent kinases 6 (CDK6) promotes the CRC cell growth. Yet the regulatory effect of miR-502-3p on CDK6 in CRC has not been reported. Thus, the primary aim of this study was to investigate whether FOXO1 enhanced miR-502-3p expression to suppress the CRC cell growth by targeting CDK6. Here, RNA level and protein level were detected by quantitative reverse transcription-PCR (qRT-PCR) and western blot (WB), respectively. Besides, the cell growth was detected by Cell Counting Kit 8 (CCK8) assay. Moreover, the regulatory effect of FOXO1 on miR-502-3p or miR-502-3p on CDK6 was determined using dual-luciferase reporter gene (DLR) assay. Results revealed that miR-502-3p and FOXO1 were downregulated in CRC cells. Besides, miR-502-3p suppressed the CRC cell growth. Moreover, FOXO1 could increase the miR-502-3p level through facilitating MIR502 transcription in CRC cells. In addition, miR-502-3p could suppress the CRC cell growth by targeting CDK6. These findings indicated that FOXO1 induced miR-502-3p expression to suppress the CRC cell growth through targeting CDK6, which might provide new therapeutic targets for CRC.

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Section: Discussionmentioning

confidence: 99%

FOXO1-Induced miR-502-3p Suppresses Colorectal Cancer Cell Growth through Targeting CDK6

Fan

Zhao

et al. 2023

Journal of Oncology

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“…This result was consistent with the result reported by Liu and Huang [ 10 ] that knocking down SNHG15 inhibited the proliferation of osteoclasts. What is more, SNHG15 has been reported to regulate the proliferation and metastatic of oral squamous cell carcinoma [ 25 ], ovarian cancer [ 26 ], and bladder cancer [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

lncRNA SNHG15 as a ceRNA modulates Osteoclast Differentiation, Proliferation, and Metastasis by Sponging miR-381-3p/NEK2 Axis

Wang

Zhu

Fang

et al. 2022

Journal of Immunology Research

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Background. A growing number of studies have shown that long noncoding RNAs play an important role in osteoclast differentiation. However, there are few studies on the roles of lncRNA small nucleolar RNA host gene 15 (SNHG15) in osteoclast differentiation. Methods. The expressions of SNHG15, miR-381-3p, and never in mitosis-related kinase 2 (NEK2) mRNA were detected by real-time quantitative polymerase chain reaction (RT-qPCR); Western blot detected NEK2 and osteoclast markers (Cathepsin K, CTSK), matrix metalloproteinase 9 (MMP9), nuclear factor of activated T cell 2 (NFAT2), and tartrate-resistant acid phosphatase (TRAP) protein levels; cell proliferation was detected by Cell Counting Kit-8 (CCK-8), and the formation of osteoclasts was observed by TRAP staining; the F-actin skeleton was stained with tetramethylrhodamine isothiocyanate (TRITC) phalloidin; cell migration rate was detected by Transwell; dual-luciferase reporter gene assay and RNA-binding protein immunoprecipitation (RIP) assay verified the targeting relationship between miR-381-3p, SNHG15, and NEK2. Results. The expression of SNHG15 was increased in THP-1 cells stimulated by macrophage colony-stimulating factor (M-CSF)/receptor activator of nuclear factor-kappa B ligand (RANKL). Overexpression of SNHG15 significantly promoted the proliferation, migration, osteoclast differentiation, and expression of osteoclast markers CTSK, MMP9, NFAT2, and TRAP of THP-1 cells induced by M-CSF/RANKL. Knockdown of SNHG15 reversed this effect. Overexpression of SNHG15 downregulated the inhibitory effect of overexpression of miR-381-3p on the proliferation, migration, and differentiation of THP-1 cells induced by M-CSF/RANKL. Knockdown of miR-381-3p reversed the inhibitory effect of knockdown of NEK2 on the proliferation, migration, and differentiation of THP-1 cells induced by M-CSF/RANKL. Conclusion. SNHG15 acted as a ceRNA promoted the proliferation, migration, and differentiation of THP-1 cells induced by M-CSF/RANKL through sponging miR-381-3p to promote the expression of NEK2.

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“…Notably, RAB17 is a direct target of miR-370-3p. Furthermore, miR-370-3p arrests the cell cycle and promotes apoptosis of ovarian cancer cell through inhibiting CDK6 (25). SLD5, a component of the GINS complex, is crucial for DNA replication (62).…”

Section: The Biological Role Of Mir-370 In Cancermentioning

confidence: 99%

“…In ovarian cancer, miR-370-3p restrains cell proliferation and promotes apoptosis by targeting CDK6 (25). Furthermore, miR-370-3p can suppress colony formation of ovarian cancer cells via targeting RAB17 (61).…”

Section: The Biological Role Of Mir-370 In Cancermentioning

confidence: 99%

“…The potential mechanism underlying miRNA-mediated gene activation is unclear. miR-370 has been reported to affect numerous biological behaviors, such as cell proliferation (21), apoptosis (22), migration (23), invasion (24), as well as cell cycle progression (25) and cell stemness (26). Furthermore, miR-370 may affect the response of cancer cells to anticancer therapy (27).…”

Section: Introductionmentioning

confidence: 99%

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Recent findings on miR‑370 expression, regulation and functions in cancer (Review)

Wang²,

et al. 2023

Oncol Rep

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MicroRNAs (miRNAs/miRs) are a group of small non-coding RNAs that serve as post-transcriptional gene modulators. miRNAs have been demonstrated to serve a pivotal role in carcinogenesis and the dysregulated expression of miRNAs is a well-understood characteristic of cancer. In recent years, miR-370 has been established as a key miRNA in various cancers. The expression of miR-370 is dysregulated in various types of cancer and varies markedly across different tumor types. miR-370 can regulate multiple biological processes, including cell proliferation, apoptosis, migration, invasion, as well as cell cycle progression and cell stemness. Moreover, it has been reported that miR-370 affects the response of tumor cells to anticancer treatments. Additionally, the expression of miR-370 is modulated by multiple factors. The present review summarizes the role and mechanism of miR-370 in tumors, and demonstrates its potential as a molecular marker for cancer diagnosis and prognosis. Contents1. Introduction 2. The aberrant expression of miR-370 in cancer 3. The biological role of miR-370 in cancer 4. The regulation of miR-370 in cancer 5. The diagnostic and prognostic value of miR-370 in cancer 6. Conclusion

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lncRNA SNHG15 Promotes Ovarian Cancer Progression through Regulated CDK6 via Sponging miR-370-3p

Cited by 9 publications

References 30 publications

FOXO1-Induced miR-502-3p Suppresses Colorectal Cancer Cell Growth through Targeting CDK6

FOXO1-Induced miR-502-3p Suppresses Colorectal Cancer Cell Growth through Targeting CDK6

lncRNA SNHG15 as a ceRNA modulates Osteoclast Differentiation, Proliferation, and Metastasis by Sponging miR-381-3p/NEK2 Axis

Recent findings on miR‑370 expression, regulation and functions in cancer (Review)

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