MicroRNA-148a suppresses proliferation and invasion potential of non-small cell lung carcinomas via regulation of STAT3

He, Mian; Xue, Yu

doi:10.2147/ott.s123518

Cited by 27 publications

(19 citation statements)

References 38 publications

(48 reference statements)

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“…Activation of STAT3 can contribute to oncogenesis by inducing tumor angiogenesis (Siveen et al, ; Swiatek‐Machado et al, ). miR‐148a can restrain NSCLC development via regulating STAT3 (He & Xue, ). Here, we found that STAT3 was a target of miR‐17 and miR‐17 can negatively regulate STAT3 expression.…”

Section: Discussionmentioning

confidence: 99%

H19 promotes non‐small‐cell lung cancer (NSCLC) development through STAT3 signaling via sponging miR‐17

Huang

Lei

et al. 2018

Journal Cellular Physiology

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LncRNAs can exhibit crucial roles in the development of multiple cancers, including non-small cell lung cancer (NSCLC). Currently, we investigated the role of lncRNA H19 in NSCLC. In our study, it was found that H19 was upregulated in A549 and H1299 cells compared to normal lung epithelial BEAS-2B cells. Meanwhile, we observed that miR-17 was downregulated in NSCLC cell lines. Inhibited H19 can suppress the growth, migration, and invasion of NSCLC cells and bioinformatics search was performed to predict the correlation between H19 and miR-17. Overexpression of miR-17 was able to inhibit the progression of NSCLC cells while reversely miR-17 inhibitors reversed this process. In addition, signal transducers and activators of transcription (STAT3), as an mRNA target of miR-17, was presented in our research. Moreover, we discovered that H19 demonstrated its biological functions via regulating miR-17 and STAT3 in vitro. Silencing H19 greatly increased STAT3 expression by sponging miR-19 in vitro. It was hypothesized that H19 may serve as a competing endogenous RNA (ceRNA) to modulate STAT3 by attaching miR-17 in lung cancer. In summary, our findings indicated that H19/miR-17/STAT3 axis participated in NSCLC development. H19 could be regarded as a significant prognostic biomarker in NSCLC progression.

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Section: Discussionmentioning

confidence: 99%

H19 promotes non‐small‐cell lung cancer (NSCLC) development through STAT3 signaling via sponging miR‐17

Huang

Lei

et al. 2018

Journal Cellular Physiology

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“…By targeting STAT3, miR‐1181 can inhibit pancreatic cancer development and can serve as a therapeutic target (Wang, Lu et al, ). miR‐148a can restrain non‐small cell lung carcinomas via regulating STAT3 (He & Xue, ). STAT3 was demonstrated to be a direct target of miR‐125b by bioinformatics research.…”

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA MALAT1 promotes oral squamous cell carcinoma development via microRNA‐125b/STAT3 axis

Chang

2017

Journal Cellular Physiology

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Oral squamous cell carcinoma (OSCC), as the most common type of oral cancer, is responsible for almost 3% of all malignant tumors worldwide. Non-coding RNAs such as lncRNAs and microRNAs have been involved in many cancers including OSCC. Recently, lncRNA metastasis-associated lung adenocarcinoma transcript-1 (MALAT1) has been reported to play an oncogenic role in OSCC metastasis. However, the underlying mechanism of MALAT1 in regulating OSCC progression remains unclear. The aim of this study was to investigate the specific role of MALAT1 in OSCC development. It was observed that MALAT1 was upregulated in OSCC cell lines. Inhibition of MALAT1 can prevent OSCC proliferation while overexpressing MALAT1 promoted OSCC progression. In addition, bioinformatics search was used to identify that miR-125b was a direct target of MALAT1, which indicated a negative correlation between MALAT1 and miR-125b. Besides these, STAT3 was predicted as a binding target of miR-125b in OSCC. Overexpression of MALAT1 was able to suppress the tumor inhibitory effect of miR-125b mimics via upregulating STAT3. Moreover, the function of MALAT1 in OSCC development was further investigated by using in vivo assays. The established nude mice models revealed that downregulated MALAT1 greatly inhibited OSCC tumor growth and reversely upregualated MALAT1 promoted OSCC development via miR-125b/STAT3 axis, respectively. In conclusion, MALAT1 can function as a competing endogenous RNA (ceRNA) to modulate STAT3 expression by absorbing miR-125b in OSCC and could be used as a novel therapeutic target in OSCC diagnosis and treatment.

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“…Li et al (27) demonstrated that miR-148a suppressed epithelial-mesenchymal transition by targeting ROCK1 in NSCLC cells. He and Xue (15) reported that miR-148a inhibited NSCLC cell proliferation and invasion via inhibition of STAT3 expression. In the current study, E2F3 was confirmed to be a direct target gene of miR-148a in lung adenocarcinoma cells.…”

Section: Discussionmentioning

confidence: 99%

“…healthy controls. Additionally, miR-148a has been reported to serve a suppressive role in NSCLC (13)(14)(15). However, the regulatory mechanism of miR-148a in lung adenocarcinoma growth remains largely unclear.…”

Section: Microrna-148a Inhibits Cell Proliferation and Cell Cycle Promentioning

confidence: 99%

MicroRNA‑148a inhibits cell proliferation and cell cycle progression in lung adenocarcinoma via directly targeting transcription factor E2F3

Liu

Tian

2018

Exp Ther Med

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MicroRNAs (miRs) serve important roles in various human cancers, including lung adenocarcinoma. Exploring the function and regulatory mechanism of miRs underlying lung adenocarcinoma progression may contribute to identifying novel therapeutic targets and candidates. The present study aimed to examine miR-148a expression and investigate the molecular mechanisms of miR-148a in lung adenocarcinomas. The data from the current study indicated that miR-148a was significantly downregulated in lung adenocarcinoma tissues and cell lines, and low miR-148a expression was significantly associated with advanced Tumor, Node, Metastasis stages and lymph node metastasis, as well as the shorter survival time of patients. Increased miR-148a expression markedly decreased the cell proliferation, colony formation and cell cycle progression of H23 and H1975 cells. Transcription factor E2F3 (E2F3) was identified as a target of miR-148a in H23 and H1975 cells. The expression of E2F3 was negatively mediated by miR-148a in H23 and H1975 cells. In addition, E2F3 was significantly upregulated in lung adenocarcinoma tissues and cell lines, and the expression of miR-148a was inversely correlated with E2F3 expression in lung adenocarcinoma tissues. Additional experiments demonstrated that increased E2F3 expression counteracted the inhibitory effects on lung adenocarcinoma cells caused by miR-148a overexpression. In summary, the findings of the current study suggest that miR-148a may have suppressive effects on the proliferation of lung adenocarcinoma cells at least in part through directly targeting E2F3. Therefore, miR-148a may be used as a potential candidate for the treatment of lung adenocarcinoma.

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MicroRNA-148a suppresses proliferation and invasion potential of non-small cell lung carcinomas via regulation of STAT3

Cited by 27 publications

References 38 publications

H19 promotes non‐small‐cell lung cancer (NSCLC) development through STAT3 signaling via sponging miR‐17

H19 promotes non‐small‐cell lung cancer (NSCLC) development through STAT3 signaling via sponging miR‐17

Long non‐coding RNA MALAT1 promotes oral squamous cell carcinoma development via microRNA‐125b/STAT3 axis

MicroRNA‑148a inhibits cell proliferation and cell cycle progression in lung adenocarcinoma via directly targeting transcription factor E2F3

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