The Novel miR-9600 Suppresses Tumor Progression and Promotes Paclitaxel Sensitivity in Non–small-cell Lung Cancer Through Altering STAT3 Expression

Sun, Chengcao; Li, Shujun; Zhang, Feng; Zhang, Yadong; Zuo, Zhenyu; Xi, Yongyong; Wang, Liang

doi:10.1038/mtna.2016.96

Cited by 79 publications

(42 citation statements)

References 50 publications

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“…17,18 In this regard, several miRNAs have been reported to suppress or promote lung cancer cell survival or death. [19][20][21][22] Consistent with these reports, we have previously reported that miR-886-3Pwas associated with survival of SCL. 23 In the current study, we further investigated role of miR-886-3P in regulating small cell lung caner cell proliferation, migration, colony formation, mesenchymal-epithelial transition (MET), and in vivo xenograft tumor formation and growth.…”

Section: Introductionsupporting

confidence: 87%

MicroRNA-886-3P functions as a tumor suppressor in small cell lung cancer

Shen

Zhou

et al. 2018

Cancer Biology & Therapy

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Small cell lung cancer (SCLC) is a highly aggressive disease and miRNAs may play an important role in modulating SCLC progression. We have previously screened 924 miRNAs and found that miR-886-3P was negatively associated with SCLC survival. In the current study, we further investigated the role of miR-886-3P mimic in regulating SCLC cell phenotypic alteration in vitro and xenograft tumor formation in vivo. We found that transfection of miR-886-3P mimic significantly inhibited SCLC cell proliferation, migration, and colony formation, and induced mesenchymal-epithelial transition (MET) by suppressing TGF-ß1 synthesis in vitro. Furthermore, intra-tumor injection of miR-886-3P mimic lead to necrosis and suppression of tumor invasion to the surrounding tissue in the subcutaneous xenograft tumor, and intra-vein injection of miR-886-3P mimic suppressed xenograft lung cancer growth in vivo. These findings suggested that miR-886-3P functions as a tumor suppressor in SCLC and thus, it might be a potential therapeutic molecule in the treatment of lung cancer.

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Section: Introductionsupporting

confidence: 87%

MicroRNA-886-3P functions as a tumor suppressor in small cell lung cancer

Shen

Zhou

et al. 2018

Cancer Biology & Therapy

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“…Accumulating literatures have documented that miR-7, as a promising tumor suppressor, could regulate the biological behavior of human lung cancer cells 1, 12, 13. Moreover, our previous research works also showed that overexpression of miR-7 could inhibit the growth of human lung cancer cells 17, 18.…”

Section: Resultsmentioning

confidence: 81%

“…The overall 5-year survival rates for surgical resection in lung cancer patients still remain poor. Thus, it is important to identify and characterize new molecular markers and genes to develop more targeted treatment strategies to improve the clinical outcome of lung cancer 1, 2, 3. Recent evidence showed that the technique of targeted gene expression, including specific gene-promoter-operating expression and distinct delivery systems, is a crucial strategy for gene therapy against various cancers including lung cancer 4, 5, 6, 7.…”

Section: Introductionmentioning

confidence: 99%

Targeted Expression of miR-7 Operated by TTF-1 Promoter Inhibited the Growth of Human Lung Cancer through the NDUFA4 Pathway

Chen

Zhao

et al. 2017

Molecular Therapy - Nucleic Acids

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Targeted expression of gene technique is an important therapeutic strategy for lung cancer. MicroRNA-7 has been well documented as a promising tumor suppressor but never been test in specific gene-promoter-targeted expression in cancer gene therapy. Here, we first evaluated the efficacy of miR-7 expression operated by the promoter of TTF-1, a lineage-specific oncogene in lung cancer, in vitro using an eukaryotic vector of TTF-1-promoter-operated expression of miR-7 (termed as p-T-miR-7). Interestingly, using a nude mice model, the growth and metastasis of human lung cancer cells in vivo were significantly reduced in remote hypodermic injection of the p-T-miR-7 group, accompanied by increased expression of miR-7 and reduced transduction of the Akt and Erk pathway in situ. Mechanism aspect, global gene expression analysis showed that downregulation of NDUFA4, a novel target of miR-7, contributed to the effects of miR-7 expression operated by TTF-1 promoter on the growth and metastasis of human lung cancer cells, as well as altered transduction of the Akt and Erk pathway. Finally, there was no significant difference in weight or histopathology of other organs. These data provided a basis for development of novel modality of miRNA-based targeted expression therapy against clinical lung cancer.

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“…For transient transfection assays, cells were transfected with plasmids of JNK1 expression or siRNAs of JNK1 and Brf1 as described previously (Fang et al ., 2016; Sun et al , 2016B–C). Serum-free medium was added to each dish with Lipofectin-DNA or Lipofectamine 2000-siRNA complexes, and cells were further incubated for 4h.…”

Section: Methodsmentioning

confidence: 99%

Exploring a common mechanism of alcohol-induced deregulation of RNA Pol III genes in liver and breast cells

Huang

Zhang

et al. 2017

Gene

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Alcohol intake is associated with numbers of different human cancers, such as hepatocellular carcinoma (HCC) and breast cancer. However, the molecular mechanism remains to be elucidated. RNA polymerase III-dependent genes (Pol III genes) deregulation elevates cellular production of tRNAs and 5S rRNA, resulting in an increase in translational capacity, which promote cell transformation and tumor formation. To explore a common mechanism of alcohol-associated human cancers, we have comparably analyzed that alcohol causes deregulation of Pol III genes in liver and breast cells. Our results reveal that alcohol enhances RNA Pol III gene transcription in both liver and breast cells. The induction of Pol III genes caused by alcohol in ER+ breast cancer lines or liver tumor lines are significantly higher than in their non-tumor cell lines. Alcohol increases cellular levels of Brf1 mRNA and protein, which is key transcription factor and specifically regulate Pol III gene activity. Alcohol activates JNK1 to upregulate transcription of Brf1 and Pol III genes, whereas inhibition of JNK1 by SP600125 or its siRNA significantly decreases the induction of these genes. Furthermore, alcohol increases the rates of transformation of liver and breast cells, repressed JNK1 and Brf1 expression decrease transcription of Pol III genes and reduce the rates of colony formation of AML-12 and MCF-10 cells. Together, these studies support the idea that alcohol induces deregulation of Brf1 and RNA Pol III genes in liver and breast cells, which share a common signaling pathway to promote cell transformation. Through the common mechanism, alcohol-induced deregulation of RNA Pol III genes brings about greater phenotypic changes.

show abstract

The Novel miR-9600 Suppresses Tumor Progression and Promotes Paclitaxel Sensitivity in Non–small-cell Lung Cancer Through Altering STAT3 Expression

Cited by 79 publications

References 50 publications

MicroRNA-886-3P functions as a tumor suppressor in small cell lung cancer

MicroRNA-886-3P functions as a tumor suppressor in small cell lung cancer

Targeted Expression of miR-7 Operated by TTF-1 Promoter Inhibited the Growth of Human Lung Cancer through the NDUFA4 Pathway

Exploring a common mechanism of alcohol-induced deregulation of RNA Pol III genes in liver and breast cells

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