miR‑140‑3p inhibits breast cancer proliferation and migration by directly regulating the expression of tripartite motif 28

Zhou, Yu; Wang, Bo; Wang, Yu; Chen, Gaohui; Lian, Qixin; Wang, Haidong

doi:10.3892/ol.2019.10038

Cited by 42 publications

(43 citation statements)

References 25 publications

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“…On the basis of the prediction from bioinformatic tools and the data from luciferase reporter, RIP and RNA pull-down assays, miR-140-3p was confirmed as a direct target of circNTRK2. MiR-140-3p was previously demonstrated as a tumor-suppressor in some types of human malignancies, such as squamous cell lung cancer [ 24 ], breast cancer [ 25 ], hepatocellular carcinoma [ 26 ] and cervical cancer [ 27 ]. In the present study, miR-140-3p expression was down-regulated in ESCC tissues and cells, and was inversely correlated to circNTRK2 expression.…”

Section: Discussionmentioning

confidence: 99%

Circular RNA circNTRK2 facilitates the progression of esophageal squamous cell carcinoma through up-regulating NRIP1 expression via miR-140-3p

Chen

Jiang

Zhao

et al. 2020

J Exp Clin Cancer Res

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Background Esophageal squamous cell carcinoma (ESCC) is one of the most prevalent gastrointestinal malignancies with high mortality. Circular RNAs (CircRNAs) have become a research hotspot in recent years for their vital roles in cancer development and progression. This study aims to clarify the roles of circNTRK2 and its underlying molecular mechanisms in ESCC. Methods The levels of circNTRK2, miR-140-3p, and nuclear receptor-interacting protein 1 (NRIP1) mRNA were examined by qRT-PCR. The cell proliferation ability was detected via CCK-8, EdU and colony formation assays. The invasion capacity was tested by using transwell assay. The apoptotic rate was evaluated through flow cytometry. The protein levels of cleaved PARP, cleaved caspase-3, E-cadherin, vimentin, and NRIP1 were measured by western blot assay. The validation of circular structure was performed by Sanger sequencing, divergent primer PCR, and RNase R treatments. The ceRNA regulatory mechanism of circNTRK2 was observed via dual-luciferase reporter, RIP and RNA pull-down assays. The mice xenograft models were constructed to confirm the oncogenicity of circNTRK2 in ESCC in vivo. Results CircNTRK2 was highly expressed in ESCC tissues and cells. High expression of circNTRK2 was correlated with advanced TNM stage, lymph node metastasis and short survival. Knockdown of circNTRK2 inhibited ESCC cell proliferation, invasion and epithelial-mesenchymal transition (EMT), and accelerated apoptosis in vitro. Mechanistic assays disclosed that circNTRK2 could act as a sponge for miR-140-3p to abate its suppression on target NRIP1 expression. Moreover, miR-140-3p-induced inhibitory effects on ESCC cell malignant phenotypes were attenuated by the overexpression of circNTRK2. In addition, depletion of NRIP1 impeded cell proliferation, invasion and EMT, while enhanced apoptosis. Furthermore, silencing of circNTRK2 suppressed cell proliferation and invasion through regulating NRIP1 expression. Also, knockdown of circNTRK2 slowed ESCC tumor growth in vivo. Conclusion CircNTRK2 promoted ESCC progression by regulating miR-140-3p/NRIP1 pathway. Our findings contribute to a better understanding of circRNAs as miRNA sponges and highlight a promising therapy target in ESCC.

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Section: Discussionmentioning

confidence: 99%

Circular RNA circNTRK2 facilitates the progression of esophageal squamous cell carcinoma through up-regulating NRIP1 expression via miR-140-3p

Chen

Jiang

Zhao

et al. 2020

J Exp Clin Cancer Res

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“…miR-140-3p enhances the sensitivity of LUAD cells to cisplatin. miR-140-3p has been reported to serve as a key tumor suppressor in several types of malignancies, where patients with lower miR-140-3p expression levels had poor prognoses (28)(29)(30)(31)33). Therefore, the present study hypothesized that upregulated miR-140-3p expression may be beneficial for the treatment of patients with LUAD.…”

Section: Reverse Transcription-quantitative Pcr (Rt-qpcr)mentioning

confidence: 88%

“…In addition, miR-708-5p has been revealed to suppress stem cell-like phenotypes in lung cancer by repressing the Wnt/β-catenin signaling pathway (26). Previous studies have suggested that upregulated miR-140-3p expression was significantly associated with reduced cell proliferation, invasion, migration and sorafenib resistance in a variety of tumors (27)(28)(29)(30). It was also reported previously that miR-140-3p expression was downregulated in lung squamous cell carcinoma (LUSC) (31), where it has been demonstrated to function as a tumor suppressor (32).…”

Section: Introductionmentioning

confidence: 99%

miR‑140‑3p enhances cisplatin sensitivity and attenuates stem cell‑like properties through repressing Wnt/β‑catenin signaling in lung adenocarcinoma cells

Wang

Pan

et al. 2020

Exp Ther Med

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Lung adenocarcinoma (LUAD) is the most predominant subtype of non-small cell lung cancer (NSCLC) that is experiencing the fastest growth rate in incidence. Chemoresistance and the presence of cancer stem cells are considered to be the main obstacles preventing the successful treatment of patients with NSCLC, the molecular mechanism of which remains poorly understood. The present study aimed to investigate the effects of microRNA (miR)-140-3p on cisplatin sensitivity and stem cell-like properties of LUAD cells. Analysis of publicly available data demonstrated that miR-140-3p expression was downregulated in LUAD, and positively associated with the overall survival rate of patients. In addition, transfection with the miR-140-3p mimic reduced LUAD cell viability and induced apoptosis following treatment with cisplatin whilst decreasing stem cell-like properties. miR-140-3p overexpression was also found to attenuate cisplatin resistance and reduce stem cell-like properties in LUAD cells by suppressing Wnt/β-catenin signaling, all of which were reversed by the overexpression of β-catenin. Taken together, results of the present study suggest miR-140-3p to be an effective therapeutic strategy for patients with LUAD.

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“…Miles et al pointed out that miR-140-3p level was reduced in ovarian cancer tumor specimens [24]. Besides, miR-140-3p was reported to be downregulated in BC, and miR-140-3p restoration could restrain BC cell growth and migration through regulating TRIM28 [15]. Consistent with these results, we demonstrated that the abundance of miR-140-3p was decreased in BC cells and tissues, and low level of miR-140-3p was closely related to advanced tumor stage.…”

Section: Accepted Articlementioning

confidence: 99%

“…MiRNAs are a class of ncRNAs (~ 22 nucleotides) that negatively modulate the expression of target genes via directly binding to the 3'UTR of target mRNAs, and miRNAs were reported as key regulators in multiple cancers [12,13]. Previous reports have shown that miR-140-3p usually serves as a tumor-suppressive miRNA in some cancers, including BC [14,15]. Nevertheless, the association between circ_0008039 and miR-140-3p in BC remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Circ_0008039 supports breast cancer cell proliferation, migration, invasion, and glycolysis by regulating the miR‐140‐3p/SKA2 axis

et al. 2020

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Circular RNAs (circRNAs) have been shown to modulate gene expression and participate in the development of multiple malignancies. The purpose of this study was to investigate the role of circ_0008039 in breast cancer (BC). The expression of circ_0008039, miR-140-3p and spindle and kinetochore-associated protein 2 (SKA2) was detected by qRT-PCR. Cell viability, colony formation, migration and invasion were evaluated using methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay, colony formation assay, and transwell assay, respectively. Glucose consumption and lactate production were measured using commercial kits. Protein levels of hexokinase II (HK2) and SKA2 were determined by western blot. The interaction between miR-140-3p and circ_0008039 or SKA2 was verified by dual-luciferase reporter assay. Finally, a mouse xenograft model was established to investigate the roles of circ_0008039 in BC in vivo. We found that circ_0008039 and SKA2 were upregulated in BC tissues and cells, while miR-140-3p was downregulated. Knockdown of circ_0008039 suppressed BC cell proliferation, migration, invasion, and glycolysis. Moreover, miR-140-3p could bind to circ_0008039 and its inhibition reversed the inhibitory effect of circ_0008039 interference on proliferation, migration, invasion, and glycolysis in BC cells. SKA2 was verified as a direct target of miR-140-3p and its overexpression partially inhibited the suppressive effect of miR-140-3p restoration in BC cells. Additionally, circ_0008039 positively regulated SKA2 expression by sponging miR-140-3p. Consistently, silencing circ_0008039 restrained tumor growth via increasing miR-140-3p and decreasing SKA2. In conclusion, circ_0008039 downregulation suppressed BC cell proliferation, migration, invasion, and glycolysis partially through regulating the miR-140-3p/SKA2 axis, providing an important theoretical basis for treatment of BC.

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miR‑140‑3p inhibits breast cancer proliferation and migration by directly regulating the expression of tripartite motif 28

Cited by 42 publications

References 25 publications

Circular RNA circNTRK2 facilitates the progression of esophageal squamous cell carcinoma through up-regulating NRIP1 expression via miR-140-3p

Circular RNA circNTRK2 facilitates the progression of esophageal squamous cell carcinoma through up-regulating NRIP1 expression via miR-140-3p

miR‑140‑3p enhances cisplatin sensitivity and attenuates stem cell‑like properties through repressing Wnt/β‑catenin signaling in lung adenocarcinoma cells

Circ_0008039 supports breast cancer cell proliferation, migration, invasion, and glycolysis by regulating the miR‐140‐3p/SKA2 axis

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