Yiqi Chutan Tang Reduces Gefitinib‐Induced Drug Resistance in Non‐Small‐Cell Lung Cancer by Targeting Apoptosis and Autophagy

Zhang, Jue; Sun, Lingling; Cui, Jingang; Wang, Jing; Liu, Xiaomin; Aung, Thazin Nwe; Qu, Zhibo; Chen, Zhuangzhong; Adelson, David L.; Lin, Lizhu

doi:10.1002/cyto.a.23869

Cited by 16 publications

(13 citation statements)

References 25 publications

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“…Several studies have proved that gefitinib exerts anticancer activity in multiple types of human cancer, including non‐small cell lung cancer, and ESCC (Sasatani et al, 2019; Schueler et al, 2019; Zhang et al, 2019). But, the resistance to gefitinib treatment is a major obstacle to the effective treatment of patients with ESCC.…”

Section: Discussionmentioning

confidence: 99%

Restoration of circPSMC3 sensitizes gefitinib‐resistant esophageal squamous cell carcinoma cells to gefitinib by regulating miR‐10a‐5p/PTEN axis

Zhu

Cao

2020

Cell Biology International

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Circular RNAs (circRNAs) has been shown to play an important role in the progression of various cancers. However, the function and underlying mechanisms of circRNAs affecting chemotherapy resistance in esophageal squamous cell carcinoma (ESCC) remain largely unknown. In this study, we used gefitinib‐resistant (GR) ESCC cells to investigate the function of circPSMC3 and clarify the underlying mechanism in chemotherapy resistance in ESCC. The results suggested that circPSMC3 expression was downregulated, but miR‐10a‐5p was upregulated in ESCC tissues and cells, as well as in GR ESCC cells. CircPSMC3 overexpression increased the sensitivity of ESCC cells to gefitinib, as indicated by reduced half maximal inhibitory concentration value, increased apoptosis rate and cleaved caspase‐3 protein expression. CircPSMC3 directly interacted with miR‐10a‐5p and inhibited the expression of miR‐10a‐5p. Phosphatase and tensin homolog (PTEN) was a direct target of miR‐10a‐5p and circPSMC3 promoted PTEN expression via decreasing miR‐10a‐5p level. Moreover, the effect of circPSMC3 on resistance of GR ESCC cells to gefitinib was remarkably reduced by restoration of miR‐10a‐5p and downregultion of PTEN. Taken together, these observations suggested that upregulation of circPSMC3 overcame resistance of GR ESCC cells to gefitinib by modulating the miR‐10a‐5p/PTEN axis, which provide a new therapeutic strategy for overcoming gefitinib resistance in ESCC.

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Section: Discussionmentioning

confidence: 99%

Restoration of circPSMC3 sensitizes gefitinib‐resistant esophageal squamous cell carcinoma cells to gefitinib by regulating miR‐10a‐5p/PTEN axis

Zhu

Cao

2020

Cell Biology International

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“…However, nearly all patients treated with gefitinib deteriorate due to the emergence of EGFR-TKI acquired resistance, for which no effective therapy is currently available (22,23). Emerging studies have reported that certain Chinese medicines could reduce gefitinib-induced drug resistance, including TP (24,25). However, the role and mechanism of TP in gefitinib-induced drug resistance in NSCLC is unclear.…”

Section: Discussionmentioning

confidence: 99%

Triptolide inhibits epithelial‑mesenchymal transition and induces apoptosis in gefitinib‑resistant lung cancer cells

Cui

Jin

et al. 2020

Oncol Rep

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The epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI), gefitinib, is used widely to treat non-small cell lung cancer (NSCLC) with EGFR-activating mutations. Unfortunately, the acquired drug resistance promoted by epithelial-mesenchymal transition (EMT) markedly limits the clinical effects and remains a major barrier to a cure. Our previous isobaric tags for relative and absolute quantitation-based proteomics analysis revealed that the E-cadherin protein level was markedly upregulated by triptolide (TP). The present study aimed to determine whether TP reverses the gefitinib resistance of human lung cancer cells by regulating EMT. It was revealed that TP combined with gefitinib synergistically inhibited the migration and invasion of lung adenocarcinoma cell line A549; the combination treatment had a significantly better outcome than that of TP and gefitinib alone. Moreover, TP effectively increased the sensitivity of drug resistant A549 cells to gefitinib by upregulating E-cadherin protein expression and downregulating the MMP9, SNAIL, and vimentin expression levels. The dysregulated E-cadherin expression of gefitinib-sensitive cells induced gefitinib resistance, which could be overcome by TP. Finally, TP combined with gefitinib significantly inhibited the growth of xenograft tumors induced using gefitinib-resistant A549 cells, which was associated with EMT reversal and E-cadherin signaling activation in vivo. The present results indicated that the combination of TP and TKIs may be a promising therapeutic strategy to treat patients with NSCLCs harboring EGFR mutations.

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“…The last article reports on drug actions immunomonitored by high-content FCM (15,16). Parry et al investigated long-term Ibrutinib therapy in B-Cell Chronic Lymphocytic Leukemia (CLL).…”

Section: Tumors Meng Et Al Link An Increased Cxcl10 Expression and mentioning

confidence: 99%

“…The last article reports on drug actions immunomonitored by high-content FCM ( 15 , 16 ). Parry et al.…”

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Editorial: Modulation of Human Immune Parameters by Anticancer Therapies

et al. 2020

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Immunoncology is among the most important hallmarks of immunotherapy revolution of cancer medicine. Here, we compiled reviews and original research articles reflecting current developments in immunoncology. Novel therapies modulate the complex interaction between tumor and immune system (Figure 1). Multiparametric flow cytometry (FCM) is a key analytical tool contributing over 1,000 research articles/ year to the field. As a quantitative single-cell technology, FCM reliably and reproducibly identifies rare populations, detects subtle changes in modulatory signals, and assesses time-sensitive antigenic expression patterns. State-of-the-art equipment, fast sophisticated software, and flexibly labeled monoclonal antibodies allow rapid analyses with high sensitivity and specificity, even in routine applications. Lambert et al. explain how new analytes are added to the portfolio of diagnostic and research laboratories. Sample preparation, antibody titration, and appropriate controls are central in cytometric analysis and must be controlled with the necessary rigor and reproducibility (1). Although tumor cell analysis is a key application of cytometry (2, 3), this research topic is dedicated to the modulation of immune parameters, and we only included work focusing on tumorimmune-cell interaction and its disease-course impact. Dendritic cells (DCs) are crucial in tumor protection (4). Lu et al. dissect the interaction of DCs with non-small cell lung cancer (NSCLC) cells, which can induce an immunosuppressive microenvironment and evade immune surveillance. Analysis of costimulatory molecules and pro-/anti-inflammatory cytokines reveals new subpopulations of CD1c+ DCs in coculture with NSCLC. Particularly, the expression of signal molecules and pro-inflammatory cytokines are suppressed, whereas the secretion of anti-inflammatory cytokines by DCs is upregulated, suggesting that NSCLC can induce tolerogenic DCs, blocking DC-mediated anti-tumor immunity. Chemokines and their corresponding receptors play a pivotal role in orchestrating trafficking of immune cells to fulfill their next tasks. CXCL10 has been associated with T cell recruitment into

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Yiqi Chutan Tang Reduces Gefitinib‐Induced Drug Resistance in Non‐Small‐Cell Lung Cancer by Targeting Apoptosis and Autophagy

Cited by 16 publications

References 25 publications

Restoration of circPSMC3 sensitizes gefitinib‐resistant esophageal squamous cell carcinoma cells to gefitinib by regulating miR‐10a‐5p/PTEN axis

Restoration of circPSMC3 sensitizes gefitinib‐resistant esophageal squamous cell carcinoma cells to gefitinib by regulating miR‐10a‐5p/PTEN axis

Triptolide inhibits epithelial‑mesenchymal transition and induces apoptosis in gefitinib‑resistant lung cancer cells

Editorial: Modulation of Human Immune Parameters by Anticancer Therapies

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