CD44 promotes cell proliferation in non-small cell lung cancer

Hu, Bo; Ma, Yuanyuan; Yang, Yue; Zhang, Lijian; Han, Han; Chen, Jinfeng

doi:10.3892/ol.2018.8051

Cited by 38 publications

(39 citation statements)

References 25 publications

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“…In agreement with our results, Hu et al reported that knockdown of CD44 expression inhibited cell proliferation and colony formation in non-small cell lung carcinoma. 26 Additionally, CD44 silencing could suppress triple-negative breast cancer cells’ growth and migration. 27 Similar observations have also been reported in bladder cancer, malignant pleural mesothelioma as well as head and neck squamous cell carcinoma, 28 – 30 strongly suggesting new research directions based on the potential of CD44 as a prognostic biomarker and therapeutic target in GBC.…”

Section: Discussionmentioning

confidence: 99%

CD44 is overexpressed and correlated with tumor progression in gallbladder cancer

Xue

et al. 2018

CMAR

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BackgroundGallbladder cancer (GBC) is a highly lethal disease and the most common biliary tract malignant tumor with poor prognosis. Accumulating evidence indicates that cluster of differentiation 44 (CD44) is overexpressed in several malignancies and has a crucial role in the development of cancer. However, its expression and function in GBC are unclear. The aim of this study was to explore CD44 expression and its role in GBC.Materials and methodsThe expression of CD44 was measured by immunohistochemistry. Tissue microarray analysis was used to confirm the relationship between CD44 expression and clinical outcomes of GBC patients. EDU assay, colony formation assay, cell migration and invasion assay were performed to detect the functions of CD44 in GBC-SD and NOZ transfected with si-RNA.ResultsCD44 was overexpressed and associated with poor outcomes in GBC patients. The univariate and multivariate analyses confirmed that elevated CD44 was an independent prognostic factor for the OS of GBC patients. Silencing CD44 could suppress the GBC cell proliferation, migration and invasion in vitro, as well as attenuated cancer stem cell functions.ConclusionCD44 markedly correlated with aggressive tumor behaviors and contributed to the progression of GBC, which could represent a novel prognostic marker and potential therapeutic target for GBC patients.

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Section: Discussionmentioning

confidence: 99%

CD44 is overexpressed and correlated with tumor progression in gallbladder cancer

Xue

et al. 2018

CMAR

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“…It has been shown that treatment of lung adenocarcinoma A549 cell with ATRA led to the downregulation of ALDH1A1 [34]. RA can reduce the ALDH activity and CD44 expression, thus affecting cell proliferation, cancer invasiveness and sensitivity to various chemotherapy drugs [24,35,36]. ALDH1A1 has been shown to convert/oxidize retinaldehyde into retinoic acid (RA) in several tissues, and to be one of the target proteins of ATRA [15].…”

Section: Discussionmentioning

confidence: 99%

“…The existence of CSC expressing CD44 and a high ALDH1A1 activity has been demonstrated in NSCLC [21][22][23]. The ALDH1A-RA signaling is involved in cancer cell proliferation, invasiveness and sensitivity to various chemotherapy drugs [24]. Retinoic acid potentiates the chemotherapeutic effect of cisplatin by inducing differentiation of CSC in several cancers [25], and adding all-trans retinoic acid (ATRA) to chemotherapy based on paclitaxel and cisplatin as first-line treatment could increase response rate (RR) and progression-free survival (PFS) in patients with advanced NSCLC [26].…”

Section: Introductionmentioning

confidence: 99%

All-trans retinoic acid reduces cancer stem cell-like cell-mediated resistance to gefitinib in NSCLC adenocarcinoma cells

Yao

Wang

Huang³

et al. 2019

Preprint

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Background: The enrichment of cancer stem cell-like cells (CSCs) has been considered to be responsible for tumor progression after an initial response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (EGFR-TKIs) in patients with non-small cell lung adenocarcinoma (NSCLC/ADC). All-trans retinoic acid (ATRA) has been shown to potentiate cancer chemotherapy due to its ability to induce signals for CSC differentiation. We therefore investigated whether ATRA could improve the response of NSCLC/ADC cells to TKI gefitinib. Methods: Treatment of NSCLC/ADC A549 and H1650 cells with gefitinib enriched the gefitinib surviving cells (GSCs). The expression of ALDH1A1 and CD44 and the IC50 values for gefitinib were determined by flow cytometry (FCM) and crystal violet assay in GSCs and ATRA-treated GSCs, respectively. Results: GSCs showed higher expression of ALDH1A1 and CD44 and IC50 values for gefitinib than their respective parental cells, suggesting that gefitinib can lead to propagation of CSC-enriched gefitinib-resistant cells. Treatment with ATRA was found to significantly reduce the increased expression of ALDH1A1 and CD44 and the IC50 values for gefitinib in A549GSC and H1650GSC cells. Conclusion: Our findings suggest that combination treatment with ATRA prevents gefitinib-induced enrichment of ALDH1A1bright/CD44high CSCs and enhances gefitinib-induced growth inhibition of NSCLC/ADC cells. Key words: All-trans retinoic acid, ALDH1A1, CD44, EGFR tyrosine kinase inhibitors, non-small cell lung adenocarcinoma

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“…In addition, CD44 is a transmembrane glycoprotein belonging to the adhesion molecule family and serves a role in numerous physiological and pathological processes. CD44 has been demonstrated to serve a significant role in tumor invasion, metastasis and drug resistance ( 35 ). Yan et al ( 36 ) and Bourguignon et al ( 37 ) have demonstrated that CD44 is closely associated with drug resistance exhibited by colon CSCs.…”

Section: Discussionmentioning

confidence: 99%

Salvianolic acid B reverses multidrug resistance in nude mice bearing human colon cancer stem cells

et al. 2018

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Salvianolic acid B (SalB) is a water-soluble phenolic compound, extractable from Salvia miltiorrhiza, and has previously been demonstrated to reverse tumor multidrug resistance (MDR) in colon cancer cells. Cancer stem cells (CSCs) are closely associated with drug resistance. Therefore, establishing a nude mouse model bearing human colon CSCs is important for the study of the mechanisms underlying colon cancer drug resistance as well as the reversal of drug resistance. The present study aimed to establish a nude mouse model bearing human colon CSCs and to investigate the effects of SalB on the drug resistance exhibited by the nude mouse model as well as determine its underlying mechanism. Cells from two colon cancer cell lines (LoVo and HCT-116) were cultured in serum-free medium to obtain CSCs-enriched spheroid cells. Following this, nude mice were transplanted with LoVo and HCT-116 colon CSCs to establish the CSC nude mouse model, which was subsequently demonstrated to exhibit MDR. The results of the present study revealed that following treatment with SalB, the chemotherapeutic drug resistance of xenografts was reversed to a certain extent. Western blot analysis was performed to investigate the expression levels of cluster of differentiation (CD)44, CD133, transcription factor sox-2 (SOX2) and ATP-binding cassette sub-family G member 2 (ABCG2) proteins, and the results demonstrated that treatment with SalB downregulated the expression of CD44, SOX2 and ABCG2 proteins in both LoVo and HCT-116 colon CSCs xenografts. In conclusion, the results of the present study revealed that a serum-free suspension method can be performed to successfully isolate colon CSCs. In addition, a nude mice bearing colon CSCs animal model was successfully established, and associated tumors were confirmed to exhibit MDR. Furthermore, SalB was demonstrated to successfully reverse MDR in nude mice bearing LoVo and HCT-116 colon CSCs, as well as suppress the expression of CD44, SOX2 and ABCG2 proteins.

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CD44 promotes cell proliferation in non-small cell lung cancer

Cited by 38 publications

References 25 publications

CD44 is overexpressed and correlated with tumor progression in gallbladder cancer

CD44 is overexpressed and correlated with tumor progression in gallbladder cancer

All-trans retinoic acid reduces cancer stem cell-like cell-mediated resistance to gefitinib in NSCLC adenocarcinoma cells

Salvianolic acid B reverses multidrug resistance in nude mice bearing human colon cancer stem cells

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