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Biomedicines
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Molecular Research on Non-small Cell Lung Cancer
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Molecular Research on Non-small Cell Lung Cancer

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 5108

Special Issue Editor

Dr. Chuhee Lee

E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Biology, School of Medicine, 170 Hyun-Chung Ro, Yeungnam University, Daegu 42415, Republic of Korea
Interests: cancer; chemoresistance; signal transduction pathway; RTK (receptor tyrosine kinase); phytochemicals
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

There are two types of lung cancer, small-cell lung carcinoma (SCLC) and non-small cell lung carcinoma (NSCLC), but NSCLC is the first leading cause of death in terms of mortality rate. Strategies for the treatment of NSCLC patients vary widely from conventional approaches including surgical resection, radiation, and chemotherapy to emerging therapies such as target therapy focusing on various oncogenes, immunotherapy, and combinational therapy. This Special Issue focuses on “Molecular Research on Non-Small Cell Lung Cancer". Recently, various oncogenes have been found to be overexpressed in NSCLC and highly correlated with aggressiveness, epithelial-to-mesenchymal transition, and chemoresistance, since they transduce multiple signals for cell growth, survival, proliferation, invasion, migration, angiogenesis, and inhibition of apoptosis. Therefore, customized therapy targeting these oncogenes may be a potent and practical target for the successful treatment of NSCLC, and this will be the focus of this Special Issue. Review manuscripts as well as original investigations demonstrating novel therapeutic targets and candidates to be tested in clinical trials and the underlying molecular mechanisms and crosstalk of signaling with other signaling pathways will be considered for publication.

Dr. Chuhee Lee
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • non-small cell lung carcinoma
  • oncogenes
  • epithelial-to-mesenchymal transition
  • chemoresistance
  • signaling pathways
  • molecular mechanisms

Published Papers (2 papers)

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Research

14 pages, 2387 KiB  
Article
Forced Overexpression of Signal Transducer and Activator of Transcription 3 (STAT3) Activates Yes-Associated Protein (YAP) Expression and Increases the Invasion and Proliferation Abilities of Small Cell Lung Cancer (SCLC) Cells
by Ping-Chih Hsu, Jhy-Ming Li and Cheng-Ta Yang
Biomedicines 2022, 10(7), 1704; https://doi.org/10.3390/biomedicines10071704 - 14 Jul 2022
Cited by 6 | Viewed by 2087
Abstract
Background: We sought to investigate the interaction between signal transducer and activator of transcription 3 (STAT3) and the Yes-associated protein (YAP) signaling pathway in human small cell lung cancer (SCLC) cells. Methods: The STAT3-overexpressing SCLC cell lines H146 and H446 were established by [...] Read more.
Background: We sought to investigate the interaction between signal transducer and activator of transcription 3 (STAT3) and the Yes-associated protein (YAP) signaling pathway in human small cell lung cancer (SCLC) cells. Methods: The STAT3-overexpressing SCLC cell lines H146 and H446 were established by plasmid DNA transfection for in vitro and in vivo experiments. Results: Overexpression of STAT3 increased YAP protein expression in H146 and H446 cells. STAT3 overexpression significantly increased YAP mRNA expression and the mRNA expression of the YAP signaling downstream genes CTGF and CYR61 in H146 and H446 cells (p < 0.05). We showed that STAT3 overexpression promoted EMT (epithelial–mesenchymal transition) with increased matrix metalloproteinase (MMP)-2 and MMP9 expression. Transwell assays showed that STAT3 overexpression increased the invasion ability of H146 and H446 cells. In addition, STAT3-overexpressing H146 cells grew significantly more rapidly than control H146 cells in the xenograft mouse model (p < 0.05). Immunohistochemistry (IHC) staining and Western blotting (WB) showed that STAT3-overexpressing H146 tumors had increased p-STAT3 and YAP staining and protein expression compared with control tumors. Increased EMT was also observed in STAT3-overexpressed xenograft tumors. Conclusions: The results of our study suggest that the overexpression of STAT3 promotes SCLC EMT, invasion, and proliferation through the activation of the YAP signaling pathway. Full article
(This article belongs to the Special Issue Molecular Research on Non-small Cell Lung Cancer)
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19 pages, 2919 KiB  
Article
Trifluoperazine and Its Analog Suppressed the Tumorigenicity of Non-Small Cell Lung Cancer Cell; Applicability of Antipsychotic Drugs to Lung Cancer Treatment
by Joo Yeon Jeong, Haangik Park, Hong Yoo, Eun-Jin Kim, Borami Jeon, Jong Deog Lee, Dawon Kang, Changjoon Justin Lee, Sun Ha Paek, Eun Joo Roh, Gwan-Su Yi and Sang Soo Kang
Biomedicines 2022, 10(5), 1046; https://doi.org/10.3390/biomedicines10051046 - 30 Apr 2022
Cited by 7 | Viewed by 2514
Abstract
Despite significant advances in diagnostic and therapeutic technologies, lung cancer remains the leading cause of cancer-related mortality worldwide. Non-small cell lung cancer (NSCLC) accounts for approximately 85% of lung cancer cases. Recently, some antipsychotics have been shown to possess anticancer activity. However, the [...] Read more.
Despite significant advances in diagnostic and therapeutic technologies, lung cancer remains the leading cause of cancer-related mortality worldwide. Non-small cell lung cancer (NSCLC) accounts for approximately 85% of lung cancer cases. Recently, some antipsychotics have been shown to possess anticancer activity. However, the effects of antipsychotics on NSCLC need to be further explored. We examined the effects of trifluoperazine (TFP), a commonly used antipsychotic drug, and its synthetic analogs on A549 human lung cancer cells. In addition, cell proliferation analysis, colony formation assay, flow cytometry, western blot analysis, and in vivo xenograft experiments were performed. Key genes and mechanisms possibly affected by TFP are significantly related to better survival outcomes in lung cancer patients. Treatment with TFP and a selected TFP analog 3dc significantly inhibited the proliferation, anchorage-dependent/independent colony formation, and migration of A549 cells. Treatment with 3dc affected the expression of genes related to the apoptosis and survival of A549 cells. Treatment with 3dc promoted apoptosis and DNA fragmentation. In all experiments, including in vivo studies of metastatic lung cancer development, 3dc had more substantial anticancer effects than TFP. According to our analysis of publicly available clinical data and in vitro and in vivo experiments, we suggest that some kinds of antipsychotics prevent the progression of NSCLC. Furthermore, this study indicates a synthetic TFP analog that could be a potential therapeutic for lung cancer. Full article
(This article belongs to the Special Issue Molecular Research on Non-small Cell Lung Cancer)
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