miR-26b is downregulated in human tongue squamous cell carcinoma and regulates cell proliferation and metastasis through a COX-2-dependent mechanism

Cao, Jiang; Guo, Tao; Dong, Qingshan; Zhang, Jianqiang; Li, Yanfeng

doi:10.3892/or.2014.3648

Cited by 34 publications

(29 citation statements)

References 30 publications

(42 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Ectopic expression of miR‐26b suppressed the proliferation and metastasis of human TSCC cells. In addition, prostaglandin‐endoperoxide synthase‐2 (encoding COX‐2) was the functional target of miR‐26b (Table ).…”

Section: Down‐regulated Mirnas In Tongue Squamous Cell Carcinomamentioning

confidence: 99%

MicroRNA expression and its implications for diagnosis and therapy of tongue squamous cell carcinoma

2015

J Cellular Molecular Medi

View full text Add to dashboard Cite

Tongue squamous cell carcinoma (TSCC) is the most common type of oral squamous cell carcinomas and is well known for its high rate of lymph nodal metastasis. Despite the identification of many molecular mechanisms in TSCC, the number of deaths associated with TSCC increased during the past 5 years. MicroRNAs (miRNAs) are a family of small non‐coding RNA molecules, which regulate gene expression by either translational inhibition or mRNA degradation. miRNAs have been proven to be key regulators of various biological and pathological processes including cell proliferation, development and tumourigenesis. Increasing evidence has demonstrated that the deregulated miRNAs are implicated in the diagnosis and treatment of TSCC. In this review, we summarized the expressions and roles of miRNAs in TSCC and comment on the potential roles of miRNAs in diagnosis, prognosis and treatment of this malignancy.

show abstract

Section: Down‐regulated Mirnas In Tongue Squamous Cell Carcinomamentioning

confidence: 99%

MicroRNA expression and its implications for diagnosis and therapy of tongue squamous cell carcinoma

2015

J Cellular Molecular Medi

View full text Add to dashboard Cite

show abstract

“…Laryngeal squamous cell carcinoma (LSCC) is an aggressive malignancy and a very common cancer of the head and neck . Alcohol drinking and tobacco smoking were two main risk factors for LSCC .…”

Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA LOC554202 promotes laryngeal squamous cell carcinoma progression through regulating miR‐31

Yang

Wang²,

Ge³

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

Laryngeal squamous cell carcinoma (LSCC) is one aggressive malignancy and accounts for 20% of all head and neck cancer. However, the role of LOC554202 in human LSCC remains unknown. The expression level of LOC554202 and miR-31 was detected in the LSCC tiussues by using qRT-PCR. Cell growth was measured by CCK-8 assay. Flow cytometry and matrigel-coated membrane was used to detect for cell cycle and invasion respectively. We indicated that lncRNA LOC554202 expression was overexpressed in LSCC tissues compared with the paired adjacent samples and higher LOC554202 expression was associated with the advanced stage. In addition, we demonstrated that the expression level of miR-31 was downregulated in LSCC tissues compared to the paired adjacent samples and lower miR-31 expression was correlated with the advanced stage. Moreover, the expression of miR-31 was negatively correlated with the expression of LOC554202 in LSCC tissues. Ectopic expression of LOC554202 promoted LSCC cell growth, cell cyle and cell invasion and overexpression of miR-31 inhibited LSCC cell growth, cell cyle and cell invasion. Elevated expression of LOC554202 suppressed miR-31 expression and promoted RhoA expression in LSCC cell, which was a direct target gene of miR-31. Furthermore, LOC554202 increased LSCC cell growth, cell cyle and cell invasion through suppressing miR-31 expression. These results suggested that LOC554202 acted as an oncogene in the development of LSCC.

show abstract

“…However, in this study we did not examine the effects of miR‐26b on the expressions of other Bcl‐2 family members. Additionally, according to previous literature, miR‐26b can regulate multiple upstream signaling pathways of mitochondrial‐mediated apoptosis, including the NF‐κB/MMP‐9/VEGF, PTEN/PI3K/AKT, and COX‐2 pathways [21,37–39]. These activities, we assume, would also be involved in the underlying mechanism of action regarding the anti‐tumorigenic effects of miR‐26b.…”

Section: Discussionmentioning

confidence: 84%

MicroRNA‐26b suppresses tumorigenicity and promotes apoptosis in small cell lung cancer cells by targeting myeloid cell leukemia 1 protein

Shi

2018

The Kaohsiung J of Med Scie

View full text Add to dashboard Cite

The aim of this study was to investigate the role of microRNA‐26b (miR‐26b) in regulating the proliferation, migration, and apoptosis of small cell lung cancer (SCLC) cells. First, we examined the expression level of miR‐26b in human normal fetal lung fibroblasts (NFLFs) and three SCLC cell lines NCI‐H466, NCI‐H1688, and NCI‐H196. In the following experiments, the three SCLC cell lines were transfected with miR‐26b mimic and inhibitor. Cell growth and survival, as well as migration and invasion capacities were determined by MTT, colony formation, Transwell migration and invasion, and wound healing assays. Cell apoptosis, production of reactive oxygen species, and mitochondrial membrane potential were also measured in the three cell lines following various treatments. As a result, we found that the level of miR‐26b was significantly lower in SCLC cells than in NFLFs. Additionally, transfection with miR‐26b mimic could inhibit proliferation, colony formation, and migration, as well as induce apoptosis in these SCLC cell lines; while miR‐26b inhibitor showed the opposite effects. Further mechanistic experiment revealed that miR‐26b could suppress the expression of myeloid cell leukemia 1 protein (Mcl‐1) and the 3′‐untranslated region (3′‐UTR) of Mcl‐1 may be the direct binding site of miR‐26b, suggesting that the effect of miR‐26b may be mediated by targeting Mcl‐1. Collectively, our findings offer a new insight into the role of miR‐26b in the pathogenesis of SCLC, and provide primary evidence supporting the potential of miR‐26b‐based therapy for the treatment of SCLC.

show abstract

miR-26b is downregulated in human tongue squamous cell carcinoma and regulates cell proliferation and metastasis through a COX-2-dependent mechanism

Cited by 34 publications

References 30 publications

MicroRNA expression and its implications for diagnosis and therapy of tongue squamous cell carcinoma

MicroRNA expression and its implications for diagnosis and therapy of tongue squamous cell carcinoma

Long non‐coding RNA LOC554202 promotes laryngeal squamous cell carcinoma progression through regulating miR‐31

MicroRNA‐26b suppresses tumorigenicity and promotes apoptosis in small cell lung cancer cells by targeting myeloid cell leukemia 1 protein

Contact Info

Product

Resources

About