2018
DOI: 10.1186/s13046-018-0845-9
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RETRACTED ARTICLE: Exosome-mediated transfer of lncRNA PART1 induces gefitinib resistance in esophageal squamous cell carcinoma via functioning as a competing endogenous RNA

Abstract: BackgroundCurrently, resistance to tyrosine kinase inhibitors, such as gefitinib, has become a major obstacle in improving the clinical outcome of patients with metastatic and advanced-stage esophageal squamous cell carcinoma (ESCC). While cell behavior can be modulated by long non-coding RNAs (lncRNAs), the roles of lncRNAs within extracellular vesicles (exosomes) are largely unknown. Therefore, we investigated the involvement and regulatory functions of potential lncRNAs enclosed in exosomes during formation… Show more

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Cited by 164 publications
(152 citation statements)
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“…It could be packaged into exosomes and transferred to sensitive cells, thus spreading sunitinib resistance. A similar study conducted by Kang et al also confirmed the role of lncRNA in drug resistance dissemination. In that study, exosome‐mediated transfer of lncRNA PART1 was demonstrated to induce gefitinib resistance in esophageal squamous cell carcinoma.…”
Section: Exosomes Functions In Tumor Pathogenesissupporting
confidence: 71%
“…It could be packaged into exosomes and transferred to sensitive cells, thus spreading sunitinib resistance. A similar study conducted by Kang et al also confirmed the role of lncRNA in drug resistance dissemination. In that study, exosome‐mediated transfer of lncRNA PART1 was demonstrated to induce gefitinib resistance in esophageal squamous cell carcinoma.…”
Section: Exosomes Functions In Tumor Pathogenesissupporting
confidence: 71%
“…RNA pull down confirmed the binding ability between PART1 and miR‐635. Except for miR‐129 in ESCC, miR‐133a, miR‐135b, miR‐196b, and miR‐193b in oral squamous cell carcinoma, to the best of our knowledge, we first found that miR‐635 was a new target miRNA for PART1. Moreover, in the present study, we demonstrated that PART1 promoted cell proliferation, migration, and invasion of NSCLC, while knockdown of PART1 performed the opposite effects on NSCLC progression.Other lncRNAs, such as MALAT1, HOTAIR, and UCA1, that were highly expressed in NSCLC, also promoted the progression and the inhibition of these lncRNAs suppressed the progression.…”
Section: Discussionmentioning
confidence: 82%
“…Otherwise, PART1 promotes tumor progression of colorectal cancer via sponging miR‐143 and regulating DNA‐methyltransferase 3A . In esophageal squamous cell carcinoma (ESCC), PART1 is upregulated and involved in poor response to gefitinib treatment, thus functioning as a novel therapeutic target for the disease . Moreover, previous study has shown that PART1 is upregulated in NSCLC specimens with poor prognosis and is related to tumor recurrence of NSCLC .…”
Section: Introductionmentioning
confidence: 99%
“…Exosomal PART1 could be used in the clinic as a treatment selection biomarker. High PART1 expression in serum exosomes indicates gefitinib resistance [92] . Another exosomal lncRNA, H19, has also been reported to promote gefitinib resistance.…”
Section: Targeted Therapymentioning
confidence: 99%