MiRNA-16 inhibited oral squamous carcinoma tumor growth in vitro and in vivo via suppressing Wnt/&amp;beta;-catenin signaling pathway

Liu, Lijun; Jiang, Han; Zhao, Jimin; Wen, Hao

doi:10.2147/ott.s153888

Cited by 14 publications

(8 citation statements)

References 44 publications

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“…Upregulation of β-catenin expression in both MDA-miR-302/367 and SK-miR-302/367 cells by miR-16 inhibitor indicates an important role for miR-16 in regulation of β-catenin in the BC cells. Suppression of vimentin and β-catenin proteins by miR-16 has previously been reported in oral squamous cell carcinoma, 40 ovarian cancer cells, 41 chordoma cells, 42 and breast cancer cells by our group. 21 MiR-16 has been shown as an important suppressor of Wnt/β-catenin signaling pathway, 41 which targets WNT3A and Frizzled receptor gene, FZD6, as two important factors of β-catenin signaling cascade.…”

Section: Discussionsupporting

confidence: 73%

miR‐16 enhances miR‐302/367‐induced reprogramming and tumor suppression in breast cancer cells

2020

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Overexpression of either miR‐302 or miR‐302/367 cluster induces reprogramming of cancer cells and exerts tumor‐suppressive effects by induction of mesenchymal‐to‐epithelial transition, apoptosis and a less proliferative capacity. Several reports have described miR‐16 as a tumor suppressor microRNA (miRNA). Here, we studied the impact of exogenous induction of miR‐16 in MDA‐MB‐231 and SK‐BR‐3 breast cancer cells following overexpression of miR‐302/367 cluster and investigated whether transfection of these cells by a mature miR‐16 mimic could affect the reprogramming state of the cells and their tumorigenicity. miR‐16 enhanced the expression levels of OCT4A, SOX2, and NANOG, generally known as transcription or pluripotency factors, and suppressed proliferation and invasiveness of these cells. Meanwhile, inhibition of miR‐16 counteracted both the reprogramming effect and the antitumor function of miR‐302/367 in the breast cancer cells. Current results indicate that miR‐16 can work as an adjuvant to improve both cancer cell reprogramming and tumor‐suppressive function of miR‐302/367 cluster in MDA‐MB‐231 and SK‐BR‐3 cells, while its inhibition counteracts all of these effects. Combined application of miRNAs that share some common targets in cancer cell signaling pathways may provide new approaches for repression of multiple hallmarks of cancer.

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Section: Discussionsupporting

confidence: 73%

miR‐16 enhances miR‐302/367‐induced reprogramming and tumor suppression in breast cancer cells

2020

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“…Watanabe et al (49) believed that the upregulation of HMGA2 expression activated the Ras signaling pathway, leading to the development of pancreatic cancer. The Wnt signaling pathway not only played a key role in regulating embryonic development, but also its abnormal activation was closely associated with the progression of tumors (50-53). Therefore, the present study ultimately indicated that the Wnt/β-catenin pathway was the underlying mechanism.…”

Section: Discussionmentioning

confidence: 99%

HMGA2 regulates acute myeloid leukemia progression and sensitivity to daunorubicin via Wnt/β-catenin signaling

Yang

Wang

et al. 2019

Int J Mol Med

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Acute myeloid leukemia (AML) is a malignant disease with an increasing prevalence in adults and children. However, valuable molecular diagnostic research is rare. In the present study, plasmids silencing and overexpressing high-mobility group AT-hook 2 (HMGA2) were respectively transfected in HL60 and NB4 cells. The effects of HMGA2 on AML cell viability, apoptosis, migration and invasion were determined by preforming MTT, flow cytometry, wound scratch and Transwell assays, respectively. Genes associated with apoptosis and Wnt signaling were evaluated by reverse transcription-quantitative (RT-q)-PcR and western blotting. AML cell sensitivity to daunorubicin (dNR) and the regulatory effects of the Wnt signaling pathway via HMGA2 following treatment with the agonist Licl or antagonist XAV939 were detected by MTT, RT-qPcR and western blot analysis. The results revealed that the expression of HMGA2 was elevated more so in HL60, KG1, U937, Kasumi-1, THP-1 and K562 cells than in NB4 cells. Silencing HMGA2 suppressed cell viability, migration and invasion, enhanced cell apoptosis and sensitivity to dNR, and almost restored the dNR inhibitory function that was promoted by Licl treatment. In addition, low expression of HMGA2 attenuated X-linked inhibitor of apoptosis and Bcl-2 mRNA and protein levels, and upregulated the expression of Bax and cleaved-caspase-3. Furthermore, silencing HMGA2 not only decreased Wnt and non-phospho-β-catenin expressions, but also partially reversed the increased expressions of these proteins induced by Licl treatment. On the other hand, overexpression of HMGA2 exhibited the opposite results after transfection in NB4 cells. The results of the present study demonstrated that HMGA2 played important roles in driving AML progression and chemosensitivity in HL60 and NB4 cells, potentially by activating the Wnt/β-catenin signaling pathway. Therefore, it was suggested that HMGA2 may be a promising molecular marker for AML diagnosis.

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“…It is well known that Wnt signaling/β-catenin pathway dysregulation is involved in cancer genesis, including oral cancer. This pathway is accompanied by various mechanisms, such as epithelial-mesenchymal transition and involvement of various miRNAs [ 51 , 52 ]. Participation of miR-30c-5p targets in this signaling pathway as shown by the pathway enrichment analysis underlies its role in oral cancer development.…”

Section: Discussionmentioning

confidence: 99%

Salivary miR-30c-5p as Potential Biomarker for Detection of Oral Squamous Cell Carcinoma

Mehterov

Vladimirov

Sacconi³

et al. 2021

Biomedicines

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The levels of different classes of extracellular RNAs (exRNAs) remain stable in bodily fluids. The detection of either enriched or depleted specific subsets of salivary microRNAs (miRNAs) has the potential to serve as a non-invasive approach for biomarker development. Thus, salivary miRNAs have emerged as a promising molecular tool for early diagnosis and screening of oral squamous cell carcinoma (OSCC). Total RNA was extracted from saliva supernatant of 33 OSCC patients and 12 controls (discovery set), and the differential expression of 8 cancer-related miRNAs was detected by TaqMan assay. Among the screened miRNAs, miR-30c-5p (p < 0.04) was significantly decreased in OSCC saliva. The same transcriptional behavior of miR30c-5p was observed in an additional validation set. miR-30c-5p showed a significant statistical difference between cases and controls with areas under the curve (AUC) of 0.82 (95% CI: 0.71–0.89). The sensitivity and the specificity of miR-30c-5p were 86% and 74%, respectively. The target identification analysis revealed enrichment of miR-30c-5p targets in p53 and Wnt signaling pathways in OSCC. Additionally, the miR-30c-5p targets had clinical significance related to overall survival. In conclusion, these findings show that downregulated miR-30c-5p has the potential to serve as a novel, non-invasive biomarker for early OSCC detection.

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MiRNA-16 inhibited oral squamous carcinoma tumor growth in vitro and in vivo via suppressing Wnt/β-catenin signaling pathway

Cited by 14 publications

References 44 publications

miR‐16 enhances miR‐302/367‐induced reprogramming and tumor suppression in breast cancer cells

miR‐16 enhances miR‐302/367‐induced reprogramming and tumor suppression in breast cancer cells

HMGA2 regulates acute myeloid leukemia progression and sensitivity to daunorubicin via Wnt/β-catenin signaling

Salivary miR-30c-5p as Potential Biomarker for Detection of Oral Squamous Cell Carcinoma

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