miR-103/miR-195/miR-15b Regulate SALL4 and Inhibit Proliferation and Migration in Glioma

Chen, Liping; Zhang, Nana; Ren, Xue-Qing; He, Jié; Liu, Yu

doi:10.3390/molecules23112938

Cited by 51 publications

(39 citation statements)

References 42 publications

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“…For example, Zheng et al showed the increased level of miR‐103 in colorectal cancer cells, and miR‐103 inhibition obviously suppressed the cell viability, migration, and invasion in vitro . Conversely, in glioma and non–small cell lung cancer, miR‐183 was downregulated and functions as the tumor suppressor. Our findings suggested that overexpression of miR‐103 may be useful to increase NPC cell viability, migration, and invasion.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐103 promotes nasopharyngeal carcinoma through targeting TIMP‐3 and the Wnt/β‐catenin pathway

Zhao

Wang

2019

The Laryngoscope

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Objectives/Hypothesis To verify how microRNA‐103 (miR‐103) is involved in nasopharyngeal carcinoma (NPC) development. Study Design Research on the relationship between miR‐103 and NPC. Methods Tissue inhibitor of metalloproteinases‐3 (TIMP‐3) was identified as the theoretical target gene of miR‐103, and its regulatory mechanism in NPC was explored by quantitative reverse transcription polymerase chain reaction, Western blot, MTT, transwell, and luciferase reporter assays. Results MiR‐103 was upregulated whereas TIMP‐3 was markedly decreased in NPC tissue samples. Ectopic expression of miR‐103 promoted NPC cell viability, migration, and invasion. In vitro assay showed that TIMP‐3 recovered miR‐103–mediated promotion of NPC cell viability, migration, and invasion. The expression of Wnt/β‐catenin pathway markers (β‐catenin and cyclin D1) were enhanced after miR‐103 overexpression. Conclusions MiR‐103 might play a key role in NPC carcinogenesis by targeting TIMP‐3 and affecting the Wnt/β‐catenin pathway. Level of Evidence NA Laryngoscope, 130:E75–E82, 2020

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Section: Discussionmentioning

confidence: 99%

MicroRNA‐103 promotes nasopharyngeal carcinoma through targeting TIMP‐3 and the Wnt/β‐catenin pathway

Zhao

Wang

2019

The Laryngoscope

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“…In particular, miR-195-5p may inhibit cell proliferation and induce apoptosis in glioma cells through the regulation of cell apoptosis-related proteins including Caspase-3, -8, -9 and Bcl-2 (34). Direct targets of miR-195 in glioma cells were identified as Sal-like protein 4 (35), cyclin E1 (36) to affect cell cycle (37) in the previous studies. The present study also demonstrated that miR-195-5p expression is reduced in glioma tissues and cells, and inhibition of miR-195-5p promoted cell proliferation, migration and invasion of glioma cells, and inhibited apoptosis.…”

Section: Discussionmentioning

confidence: 90%

Long non‑coding RNA LINC00473/miR‑195‑5p promotes glioma progression via YAP1‑TEAD1‑Hippo signaling

Wang

et al. 2019

Int J Oncol

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There is an urgent need to identify novel potential therapeutic targets for diagnosis and treatment of glioma, a common primary tumor in brain, due to its high-level invasiveness. Long non-coding RNA (lncRNA) LINC00473 has been reported as potentially critical regulators in various types of cancer tumorigenesis. However, the effects of LINC00473 on glioma cells is unclear. The present study aimed to investigate the clinical significance, effects and mechanism of LINC00437 on glioma tumorigenesis. In the present study, LINC00473 was significantly increased in glioma tissues and in cell models, and predicted a poor prognosis in patients with glioma. Notably, LINC00473 knockdown not only suppressed cell proliferation, invasion and migration of glioma cells, but also blocked cell cycle progression and induced apoptosis. Subcutaneous xenotransplanted tumor model experiments revealed that reduced LINC00473 expression was able to suppress in vivo glioma growth. Mechanistically, LINC00473 functioned as a competing endogenous (ce)RNA to decrease microRNA (miR)-195-5p expression. Moreover, Yes-associated protein 1 (YAP1) and TEA domain family member 1 (TEAD1) were identified as downstream targets of miR-195-5p, whose expression levels were inhibited by miR-195-5p. LINC00473 knockdown suppressed glioma progression through the decrease of miR-195-5p and subsequent increase of YAP1 and TEAD1 expression levels. These results indicated LINC00473 might act as a ceRNA to sponge miR-195-5p, thus promoting YAP1 and TEAD1 expressions, and shedding light on the underlying mechanisms of LINC00473-induced glioma progression.

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“…For example, decreased miR-195 expression in hepatocellular carcinoma tissues significantly promotes proliferation, invasion and tumorigenesis (26). Moreover, miR-195 represses cell proliferation, migration and invasion, and accelerates apoptosis in glioma by decreasing spalt like transcription factor 4 protein expression (27). downregulation of miR-195 in colon carcinoma tissues is also associated with increased cell proliferation, migration and invasion (28).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑195 suppresses cell proliferation, migration and invasion in epithelial ovarian carcinoma via inhibition of the CDC42/CCND1 pathway

et al. 2020

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Epithelial ovarian carcinoma (EOc) is the most common cause of gynecological cancer mortality, and poses a threat to women. MicroRNA-195 (miR-195) has been reported to induce apoptosis of human OVcAR-3 cells by inhibiting the VEGFR2/AKT pathway. However, the role of miR-195 in EOc remains unknown. A previous study reported that cell division cycle 42 (cdc42) can serve as a target gene of miR-195 and mediate malignant progression of esophageal squamous cell carcinoma (EScc). The aim of the present study was to investigate the role of miR-195 in EOc and the regulation in cdc42/ccNd1 pathway. Tissues samples and clinical materials were collected from 78 enrolled patients with EOC to analyze the expression and clinical significance of miR-195, cdc42 and cyclin d1 (ccNd1). Human EOc cell lines OVcA420, OVcAR-3, A2780 and SKOV3 cell lines were used to assess the expression and function of miR-195, cdc42 and ccNd1 in vitro. cell proliferation, the cell cycle and apoptosis, as well as the cell migratory and invasive abilities were detected in vitro using BrdU incorporation, colony formation, wound healing and Transwell invasion assays, along with flow cytometry. miR-195 was downregulated, while CDC42 and ccNd1 were upregulated in human EOc tissues and cells, and the aberrant expression of both was associated with increased EOc malignancy. Moreover, miR-195 expression was negatively correlated with cdc42 and ccNd1 expression levels, and negatively regulated these expression levels. Thus, it was suggested that miR-195 functions as a tumor suppressor, but cdc42 and ccNd1 act as tumor promoters based their abilities to enhance cell proliferation, cell cycle entry, migration and invasion, as well as decrease apoptosis in OVcAR-3 cells. the present results demonstrated that miR-195 inhibited human EOc progression by downregulating cdc42 and CCND1 expression. Furthermore, it was identified that miR-195, cdc42 and ccNd1 may be effective biomarkers for EOc diagnosis and treatment.

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miR-103/miR-195/miR-15b Regulate SALL4 and Inhibit Proliferation and Migration in Glioma

Cited by 51 publications

References 42 publications

MicroRNA‐103 promotes nasopharyngeal carcinoma through targeting TIMP‐3 and the Wnt/β‐catenin pathway

MicroRNA‐103 promotes nasopharyngeal carcinoma through targeting TIMP‐3 and the Wnt/β‐catenin pathway

Long non‑coding RNA LINC00473/miR‑195‑5p promotes glioma progression via YAP1‑TEAD1‑Hippo signaling

MicroRNA‑195 suppresses cell proliferation, migration and invasion in epithelial ovarian carcinoma via inhibition of the CDC42/CCND1 pathway

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