Abstract
Pulmonary carcinoma is a main cause of cancer death internationally. Chemotherapeutic regimens in most solid tumors have limited effect. And in the targeted inhibition of carcinogenic driver mutations with molecular therapies, in a large number of cases, patients acquire resistance to drugs. Therefore, the development of new therapeutic approaches is highly desirable. In the present study, we evaluated the applicability of 4[(5,6,7,8-tetrahydro-5,5,8,8- tetramethyl- 2-naphthalenyl)carbamoyl]benzoic acid (Am80), a synthetic retinoid, as a differentiation inducer in pulmonary carcinoma and examined its effect on the viability and differentiation of Calu-6 cells (a human nonsmall cell lung cancer cell line), with the final goal of establishing a new approach to pulmonary carcinoma therapy. The cell viability of Calu-6 cells after Am80 treatment was assessed by the CellTiter-Glo Luminescent Cell Viability Assay. The early apoptosis of cells was detected by Terminal deoxynucleotidyl Transferase-mediated deoxyuridine triphosphate Nick End Labeling (TUNEL) staining. The differentiation-inducing effect of Am80 on Calu-6 cells was investigated by immunostaining. Am80 induced the differentiation of Calu-6 to alveolar type I and II cells. However, Am80 reduced the viability of Calu-6 cells without inducing apoptosis. In addition, in order to investigate whether Am80 inhibits tumor growth in vivo, we conducted an in vivo experiment to determine he effect of the intratumoral administration of Am80 in mice harboring sc tumors composed of Calu-6 cells. Am80 significantly influenced the suppression of tumor growth.
Highlights
Pulmonary carcinoma is a main cause of cancer death internationally [1]
We previously demonstrated the antiproliferative effects of Am80 in A549 cells; we were unable to confirm whether Am80 induced the differentiation of pulmonary adenocarcinoma [14]
In order to evaluate the adaptability of Am80 as a differentiation inducer in pulmonary carcinoma, with the final goal of providing a new approach to pulmonary carcinoma therapy, we examined its effect on the viability and differentiation of a human non-small cell lung cancer (NSCLC) cell line, Calu-6
Summary
Pulmonary carcinoma is a main cause of cancer death internationally [1]. Non-small cell lung cancer (NSCLC) accounts for about 85% of all pulmonary carcinoma cases. Pulmonary carcinomas are categorized into three histological subtypes: adenocarcinoma, squamous cell carcinoma, and large cell carcinoma [2]. Pulmonary adenocarcinoma, which accounts for about 40% of all pulmonary carcinomas, is currently the main histological type and its incidence has increased gradually [4]. The targeted inhibition of carcinogenic driver mutations with molecular therapies, such as epidermal growth factor receptor and the anaplastic lymphoma kinase, has brought spectacular improvements in the overall survival in defined subsets of patients [5]. In a large number of cases, patients acquire resistance to these drugs due to secondary mutations and other mechanisms [6]
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