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Primary research
Long non coding RNA CCAT2 enhances the proliferation, migration, invasion and drug-resistances of non-small lung cancer via activating the miR-204-3p-suppresed IGFBP2/AKT/Bcl2 pathway
Yanfeng Huang
Department of thoracic surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute. Shenyang 110042
Corresponding Author
ORCiD: https://orcid.org/0000-0002-4576-0105
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Background: To date, the treatment efficacy of NSCLC remains unsatisfactory mainly ascribed to the rapid progress, high rate of metastasis, and emerged drug-resistance. It has been demonstrated that aberrant expression of long non coding RNA colon cancer-associated transcript 2 (CCAT2) was closely related to tumorigenesis and development of drug-resistance of many cancer types. The present study was aimed to thoroughly investigate the effect of CCAT2 in the progress of NSCLC and the underlying mechanisms, so that provide valuable theoretical basis for efficient treatment of NSCLC.
Methods: The expressions of CCAT2 were determined using the RT-qPCR experiment. Its target genes and downstream molecules were respectively evaluated by Western-blot assay and RT-qPCR experiment. Cell growth of NSCLC cells was investigated using the CCK-8 kit. The effect of CCAT2 on the progress of NSCLC and the underlying mechanisms in vivo was determined on the NSCLC-bearing mice models.
Results: Higher expression of CCAT2 was detected in the lung cancer tissues and cells than the normal ones. Moreover, it was revealed that aberrant expression of CCAT2 in lung cancer signally contributed to proliferation, invasion, and migration of cancer cells and the progress of tumor tissues. Additionally, high level of CCAT2 dramatically down-regulated the cytotoxicity of cisplatin (DDP) to NSCLC cells and tissues by upregulation of the drug-resistance related proteins. Mechanisms studies displayed that upregulation of CCAT2 markedly decreased the miR-204-3p while contrary result was obtained when down-regulated the CCAT2 level. We further demonstrated that down-regulation of miR-204-3p level signally enhanced the activity of the insulin-like growth factor (IGF) signaling pathway.
Conclusions: The CCAT2 promoted the progress and drug-resistance of NSCLC thorough activation of the miR-204-3p suppressed IGFBP2/AKT/Bcl2 pathway, and may provide theoretical basis for improvement of therapy of NSCLC.
Keywords
non-small cell lung cancer, colon cancer-associated transcript 2, IGF-binding protein, miR-204-3p, drug-resistance
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Primary research
Long non coding RNA CCAT2 enhances the proliferation, migration, invasion and drug-resistances of non-small lung cancer via activating the miR-204-3p-suppresed IGFBP2/AKT/Bcl2 pathway
Yanfeng Huang
Department of thoracic surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute. Shenyang 110042
Corresponding Author
ORCiD: https://orcid.org/0000-0002-4576-0105
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 2
Posted 17 Jun, 2020
No community comments so far
No comments provided
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cancer Biology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: To date, the treatment efficacy of NSCLC remains unsatisfactory mainly ascribed to the rapid progress, high rate of metastasis, and emerged drug-resistance. It has been demonstrated that aberrant expression of long non coding RNA colon cancer-associated transcript 2 (CCAT2) was closely related to tumorigenesis and development of drug-resistance of many cancer types. The present study was aimed to thoroughly investigate the effect of CCAT2 in the progress of NSCLC and the underlying mechanisms, so that provide valuable theoretical basis for efficient treatment of NSCLC.
Methods: The expressions of CCAT2 were determined using the RT-qPCR experiment. Its target genes and downstream molecules were respectively evaluated by Western-blot assay and RT-qPCR experiment. Cell growth of NSCLC cells was investigated using the CCK-8 kit. The effect of CCAT2 on the progress of NSCLC and the underlying mechanisms in vivo was determined on the NSCLC-bearing mice models.
Results: Higher expression of CCAT2 was detected in the lung cancer tissues and cells than the normal ones. Moreover, it was revealed that aberrant expression of CCAT2 in lung cancer signally contributed to proliferation, invasion, and migration of cancer cells and the progress of tumor tissues. Additionally, high level of CCAT2 dramatically down-regulated the cytotoxicity of cisplatin (DDP) to NSCLC cells and tissues by upregulation of the drug-resistance related proteins. Mechanisms studies displayed that upregulation of CCAT2 markedly decreased the miR-204-3p while contrary result was obtained when down-regulated the CCAT2 level. We further demonstrated that down-regulation of miR-204-3p level signally enhanced the activity of the insulin-like growth factor (IGF) signaling pathway.
Conclusions: The CCAT2 promoted the progress and drug-resistance of NSCLC thorough activation of the miR-204-3p suppressed IGFBP2/AKT/Bcl2 pathway, and may provide theoretical basis for improvement of therapy of NSCLC.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6