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      Targeting claudin-3 suppresses stem cell-like phenotype in nonsquamous non-small-cell lung carcinoma

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          Abstract

          Aim:

          To determine the role of claudin-3 in cancer stemness in nonsquamous non-small-cell lung carcinoma (NSCLC).

          Materials & methods:

          In vitro/vivo extreme limiting dilution analysis and the side population assay were used to investigate the role of claudin-3 in regulating cancer stemness in nonsquamous NSCLC.

          Results & conclusion:

          Claudin-3 depletion decreased the formation rates of spheres and tumors and increased cisplatin sensitivity. Claudin-3 was also identified as one downstream target of estrogen receptor-α in regulating cancer stemness. Moreover, targeting CLDN-3 transcription by small molecules including withaferin A, estradiol and fulvestrant suppressed cancer stemness and reversed chemoresistance. These results demonstrated claudin-3 is one positive regulator of cancer stemness in nonsuqamous NSCLC.

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          Most cited references41

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          Structure and function of claudins.

          Gerd Krause, Lars Winkler, Sebastian Mueller … (2008)
          Claudins are tetraspan transmembrane proteins of tight junctions. They determine the barrier properties of this type of cell-cell contact existing between the plasma membranes of two neighbouring cells, such as occurring in endothelia or epithelia. Claudins can completely tighten the paracellular cleft for solutes, and they can form paracellular ion pores. It is assumed that the extracellular loops specify these claudin functions. It is hypothesised that the larger first extracellular loop is critical for determining the paracellular tightness and the selective ion permeability. The shorter second extracellular loop may cause narrowing of the paracellular cleft and have a holding function between the opposing cell membranes. Sequence analysis of claudins has led to differentiation into two groups, designated as classic claudins (1-10, 14, 15, 17, 19) and non-classic claudins (11-13, 16, 18, 20-24), according to their degree of sequence similarity. This is also reflected in the derived sequence-structure function relationships for extracellular loops 1 and 2. The concepts evolved from these findings and first tentative molecular models for homophilic interactions may explain the different functional contribution of the two extracellular loops at tight junctions.
          Article 0 comments Cited 229 times – based on 0 reviews     Review now
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            Claudin proteins in human cancer: promising new targets for diagnosis and therapy.

            Patrice J. Morin (2005)
            The tight junction proteins claudins are abnormally regulated in several human cancers. In particular, claudin-3 and claudin-4 are frequently overexpressed in several neoplasias, including ovarian, breast, pancreatic, and prostate cancers. Although the exact roles of these proteins in tumorigenesis are still being uncovered, it is clear that they represent promising targets for cancer detection, diagnosis, and therapy.
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              Estrogen receptor breast cancer phenotypes in the Surveillance, Epidemiology, and End Results database.

              William F Anderson, Nilanjan Chatterjee, William Ershler … (2002)
              Researchers question whether estrogen receptor alpha-negative (ERN) and -positive (ERP) represent different stages of one disease or different breast cancer types. To further examine ERalpha phenotypes, we stratified incident tumor characteristics in the Surveillance, Epidemiology, and End Results (SEER) Database (n = 82,488) by ERN and ERP. Study variables included black-white race, age-at-diagnosis, and standard incident tumor characteristics. These characteristics were arbitrarily dichotomized into good versus poor prognostic factor groups, for example, good (tumor size 2.0 cm, positive nodes, and poor grade). Age frequency density plots were generated from the corresponding age-at-diagnosis frequency histograms. Average annual age-specific incidence rates (or risks) were adjusted to the 1970 United States standard female population. Age frequency density plots demonstrated bimodal premenopausal and postmenopausal breast cancer populations. ERN was correlated with premenopausal disease, black race, and poor prognostic factor groups, whereas ERP was associated with postmenopausal disease, white race, and favorable tumor characteristics. ERN rates increased premenopausally and then flattened to a nearly constant level after 50 years of age. ERP risk rose for most of a woman's lifetime with the greatest risk occurring between 75 and 79 years. ERalpha exhibited bimodal age frequency distribution with a dichotomous pattern for age-specific rates, racial, and prognostic factor profiles. Menopause had a greater effect on ERN than ERP. Possible implications for breast carcinogenesis and cancer prevention are discussed in the text.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Lung Cancer Manag
                Journal ID (iso-abbrev): Lung Cancer Manag
                Journal ID (publisher-id): LMT
                Title: Lung Cancer Management
                Publisher: Future Medicine Ltd (London, UK )
                ISSN (Print): 1758-1966
                ISSN (Electronic): 1758-1974
                Publication date Collection: February 2019
                Publication date (Electronic): 26 February 2019
                Publication date PMC-release: 26 February 2019
                Volume: 8
                Issue: 1
                Electronic Location Identifier: LMT04
                Affiliations
                [1 ]School of Materials Science & Engineering, South China University of Technology, Guangzhou 510640, China
                [2 ]R&D Center, Guangzhou Ribobio Co., Ltd, Guangzhou 510663, China
                [3 ]State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210046, China
                [4 ]Department of Radiology, Jinan Central Hospital, Jinan, Shandong 250013, China
                [5 ]Department of Respiratory Medicine, The Affiliated Jiangyin Hospital of Southeast University, Jiangyin 214400, China
                Author notes
                *Author for correspondence: Xeno.ma@ 123456163.com

                ‡Authors contributed equally

                Article
                DOI: 10.2217/lmt-2018-0010
                PMC ID: 6488947
                SO-VID: 440a7c93-5f84-4a4b-8142-43fb52625814
                Copyright © © 2019 Lin Ma
                License:

                This work is licensed under a Creative Commons Attribution-NonCommercial NonDerivative 4.0 Unported License

                History
                Date received : 08 May 2018
                Date accepted : 08 November 2018
                Date: 26 February 2019
                Categories
                Subject: Research Article

                Keywords:  cancer stemness,cisplatin,claudin-3,cscs,elda,estrogen receptor-α,nonsquamous nsclc,side population,tight junction,tumorigenesis
                Data availability:
                Keywords:  cancer stemness, cisplatin, claudin-3, cscs, elda, estrogen receptor-α, nonsquamous nsclc, side population, tight junction, tumorigenesis

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