MiR-124 Inhibits Growth and Enhances Radiation-Induced Apoptosis in Non-Small Cell Lung Cancer by Inhibiting STAT3

Wang, Mengjie; Meng, Bi; Liu, Yangchen; Yu, Jingwen; Chen, Qiaoyun

doi:10.1159/000485907

Cited by 55 publications

(36 citation statements)

References 32 publications

(30 reference statements)

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“…cell invasion and migration by targeting Janus kinase 2. In addition, CD164, LIM homeobox 2, STAT3 and snail family transcriptional repressor 2 have been identified as target genes of miR-124 in NSCLC (16,(21)(22)(23). In the present study, a luciferase reporter gene assay data confirmed that LIMD2 was a direct target gene of miR-124, and the expression of LIMD2 was negatively mediated by miR-124 in NSCLC.…”

Section: Discussionsupporting

confidence: 73%

Overexpression of LIMD2 promotes the progression of non‑small cell lung cancer

et al. 2019

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LIM domain containing 2 (LIMD2) is a small LIM-only protein that has been demonstrated to promote tumor progression; however, the expression and function of LIMD2 in non-small cell lung cancer (NSCLC) has not previously been reported. In the present study, reverse transcription-quantitative PCR and western blot analysis were conducted to examine the mRNA and protein expression levels of LIMD2. Cell Counting Kit-8, Transwell and wound-healing assays were performed in order to examine cell proliferation, invasion and migration, respectively. The data revealed that the LIMD2 expression levels were significantly increased in NSCLC tissues and cell lines, compared with adjacent non-tumor tissues and normal lung epithelial cells, respectively. In addition, the high expression of LIMD2 was significantly associated with lymph node metastasis, distant metastasis and advanced clinical stage in NSCLC. The patients with NSCLC with a high expression of LIMD2 exhibited shorter survival times than those with low LIMD2 expression. The knockdown of LIMD2 caused remarkable decreases in NSCLC cell proliferation, migration and invasion. Bioinformatics analysis and luciferase reporter gene assay data further confirmed that LIMD2 was a direct target gene of microRNA-124 (miR-124), a well-known tumor suppressor in NSCLC. The expression of LIMD2 was negatively regulated by miR-124 in NSCLC cells. In addition, miR-124 was downregulated in NSCLC tissues compared with adjacent non-tumor tissues, and an inverse correlation was observed between the expression of LIMD2 and miR-124 in NSCLC tissues. In conclusion, the present study demonstrates that LIMD2 serves an oncogenic role in NSCLC, suggesting that it may be used as a potential therapeutic target for the treatment of NSCLC.

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Section: Discussionsupporting

confidence: 73%

Overexpression of LIMD2 promotes the progression of non‑small cell lung cancer

et al. 2019

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“…We firstly investigated the roles of radiation on migration and invasion of NSCLC cells. It has been reported that radiation greater than 5 Gy can significantly inhibit the proliferation of NSCLC cells . Our data showed that the radiation of 2 Gy, which had no significant effect on cell proliferation , can significantly inhibit the wound healing of A549 (Fig.…”

Section: Resultssupporting

confidence: 48%

“…In colorectal cancer cells, miR‐451a can regulate the cell proliferation in response to radiation . It has been reported that miR‐124 can enhance the radiation‐induced apoptosis of NSCLC cells via inhibition of STAT3 . Similarly, miR‐144‐5p can enhance the radiosensitivity of NSCLC cells by regulating ATF2 .…”

Section: Introductionmentioning

confidence: 99%

miR‐155‐5p and miR‐760 mediate radiation therapy suppressed malignancy of non‐small cell lung cancer cells

et al. 2019

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MicroRNAs (miRNAs) play important roles in tumorigenesis of various cancers. Recent study suggested that miRNAs are involved in the therapeutic functions of radiation during cancer treatment. We found that radiation can decrease the migration and invasion of non-small cell lung cancer (NSCLC) cells. Mechanistically, radiation can significantly increase the expression of miR-155-5p and miR-760 in NSCLC cells. Knockdown of miR-155-5p and miR-760 can attenuate radiation suppressed proliferation of NSCLC cells. Among the various targets of miR-155-5p, radiation can decrease the expression of HIF-1α. Similarly, radiation can also suppress the expression of IL-6 via a miR-760 dependent pathway. Gain and loss of function studies confirmed that both HIF-1α and IL-6 were involved in the radiation suppressed proliferation of NSCLC cells. Collectively, our data showed that radiation can regulate the expression of miR-155-5p and miR-760 to suppress the malignancy of NSCLC cells. © 2019 BioFactors, 45(3):393-400, 2019

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“…In addition, miR‐1301 inhibits HCC cell progression by inactivating Wnt/β‐catenin signaling (Yang et al, ). miR‐1301 can suppress tumor cell migration and invasion through targeting p53/UBE4B in cancer cells (B. Wang et al, ; M. Wang et al, ). In addition, lower miR‐1301 expression results in poor survival in patients with glioma (Bai, Hu, Wang, Yin, & Shang, ).…”

Section: Discussionmentioning

confidence: 99%

LINC01433 promotes hepatocellular carcinoma progression via modulating the miR‐1301/STAT3 axis

Huang¹,

Zhang

et al. 2018

Journal Cellular Physiology

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Long noncoding RNAs (lncRNAs) have been demonstrated to play significant roles in hepatocellular carcinoma (HCC) tumor progression. LINC01433 has been implicated in the progression of lung cancer. However, its biological role in HCC remains poorly understood. In our current study, we focused on the detailed mechanism of LINC01433 in HCC development. First, it was exhibited that LINC01433 was remarkably elevated in HCC cells, which indicated that LINC01433 was involved in HCC. Then, knockdown of LINC01433 was able to restrain HCC cell proliferation and cell colony formation and greatly induced cell apoptosis. On the contrary, overexpression of LINC01433 promoted HCC cell proliferation, increased cell colony formation, and enhanced cell invasion capacity. Subsequently, we found that miR-1301 was remarkably decreased in HCC cells, and it can serve as a target of LINC01433 according to bioinformatics analysis. In addition, the binding correlation between them was validated by performing RNA pull-down experiments and RIP assay. Moreover, STAT3 was predicted and validated as a target of miR-1301, and it was shown that miR-1301 mimics significantly suppressed STAT3 in HCC cells.Finally, in vivo models were established, and the results demonstrated that silencing of LINC01433 could repress HCC development through modulating miR-1301 and STAT3. Taken together, these results indicated in our study that LINC01433 participated in HCC progression through modulating the miR-1301/STAT3 axis and it might act as a novel biomarker in HCC diagnosis and treatment.

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MiR-124 Inhibits Growth and Enhances Radiation-Induced Apoptosis in Non-Small Cell Lung Cancer by Inhibiting STAT3

Cited by 55 publications

References 32 publications

Overexpression of LIMD2 promotes the progression of non‑small cell lung cancer

Overexpression of LIMD2 promotes the progression of non‑small cell lung cancer

miR‐155‐5p and miR‐760 mediate radiation therapy suppressed malignancy of non‐small cell lung cancer cells

LINC01433 promotes hepatocellular carcinoma progression via modulating the miR‐1301/STAT3 axis

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