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Primary research
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
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
The treatment efficacy remains unsatisfactory due to the rapid progress, high rate of metastasis, and drug-resistance of NSCLS. It has been demonstrated that aberrant expression of long non coding RNA colon cancer-associated transcript 2 (CCAT2) in cells was closely related to tumorigenesis, tumor metastasis, and development of drug-resistance. The present study was aimed to thoroughly investigate the effect of CCAT2 in the growth of NSCLC and the underlying mechanisms, so that provide valuable theoretical basis for efficient treatment of NSCLC.
Methods
The expressions of CCAT2 and its target genes and downstream signals were respectively determined by Western-blot assay and RT-qPCR experiment. Cell growth of NSCLC cells was investigated using the CCK-8 kit while the proliferation assay was performed with the help of EDU staining. The NSCLC-bearing mice mode was established to evaluate the effect of PYCR1 on the progress of NSCLC and the underlying mechanisms in vivo.
Results
The CCAT2 was highly expressed in NSCLC tumor tissues and cells while not the corresponding normal ones. Further studies 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. Moreover, 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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A new preprint design is coming!
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This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Primary research
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
The most recent version of this article is available here.
No community comments so far
Version 1
Posted 03 May, 2020
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
The most recent version of this article is available here.
Background
The treatment efficacy remains unsatisfactory due to the rapid progress, high rate of metastasis, and drug-resistance of NSCLS. It has been demonstrated that aberrant expression of long non coding RNA colon cancer-associated transcript 2 (CCAT2) in cells was closely related to tumorigenesis, tumor metastasis, and development of drug-resistance. The present study was aimed to thoroughly investigate the effect of CCAT2 in the growth of NSCLC and the underlying mechanisms, so that provide valuable theoretical basis for efficient treatment of NSCLC.
Methods
The expressions of CCAT2 and its target genes and downstream signals were respectively determined by Western-blot assay and RT-qPCR experiment. Cell growth of NSCLC cells was investigated using the CCK-8 kit while the proliferation assay was performed with the help of EDU staining. The NSCLC-bearing mice mode was established to evaluate the effect of PYCR1 on the progress of NSCLC and the underlying mechanisms in vivo.
Results
The CCAT2 was highly expressed in NSCLC tumor tissues and cells while not the corresponding normal ones. Further studies 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. Moreover, 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
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