The <scp>HSP</scp>90/<scp>Akt</scp> pathway may mediate artemether‐induced apoptosis of Cal27 cells

Wu, Jianhua; Li, Lei; Wang, Yiting; Ren, Xiaobin; Lin, Ken; He, Yueqiu

doi:10.1002/2211-5463.12711

Cited by 8 publications

(3 citation statements)

References 34 publications

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“…Yamachika et al also reported that ART induces apoptosis in human gingival epithelial cells that have been immortalised and transformed by HPV 16 (Yamachika et al, 2004). Artemether, an ART derivative, has also been reported to induce apoptosis in a tongue squamous cell line (Cal27) via the HSP90/Akt pathway (Wu et al, 2019). However, in the present study, we were unable to distinguish the proportion of tumour volume reduction caused by angiogenesis inhibition.…”

Section: Discussionmentioning

confidence: 99%

Artemisinin suppressed tumour growth and induced vascular normalisation in oral squamous cell carcinoma via inhibition of macrophage migration inhibitory factor

Fan

et al. 2022

Oral Diseases

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BackgroundTumour vascular normalisation therapy advocates a balance between pro‐angiogenic factors and anti‐angiogenic factors in tumours. Artemisinin (ART), which is derived from traditional Chinese medicine, has been shown to inhibit tumour growth; however, the relationship between ART and tumour vascular normalisation in oral squamous cell carcinoma (OSCC) has not been previously reported.MethodsDifferent concentrations(0 mg/kg, 25 mg/kg, 50 mg/kg, 100 mg/kg)of ART were used to treat the xenograft nude mice model of OSCC. The effects of ART on migration and proliferation of OSCC and human umbilical vein endothelial cells (HUVEC) cells were detected by scratch assay and CCK‐8 assay. OSCC cells with macrophage migration inhibitory factor (MIF) silenced were constructed to explore the effect of MIF.ResultsTreatment with ART inhibited the growth and angiogenesis of OSCC xenografts in nude mice and downregulated vascular endothelial growth factor (VEGF), IL‐8, and MIF expression levels. ART reduced the proliferation, migration, and tube formation of HUVEC, as well as the expression of VEGFR1 and VEGFR2. When the dose of ART was 50 mg/kg, vascular normalisation of OSCC xenografts was induced. Moreover, VEGF and IL‐8 were needed in rhMIF restoring tumour growth and inhibit vascular normalisation after the addition of rhMIF to ART‐treated cells.ConclusionArtemisinin might induce vascular normalisation and inhibit tumour growth in OSCC through the MIF‐signalling pathway.

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Section: Discussionmentioning

confidence: 99%

Artemisinin suppressed tumour growth and induced vascular normalisation in oral squamous cell carcinoma via inhibition of macrophage migration inhibitory factor

Fan

et al. 2022

Oral Diseases

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“…However, HSP90 inhibitor monotherapy failed to improve the survival of patients with lung cancer, suggesting that drug resistance also limits the efficacy [ 47 ]. HSP90 forms a complex with AKT and thus modulates AKT activity [ 48 ]. Consistently, we found that STA-9090 decreased the levels of AKT, p-AKT, and p-S6 in lung cancer cells ( Figure 4(k) ).…”

Section: Discussionmentioning

confidence: 99%

Enhancing the Therapeutic Efficacy of KRASG12C Inhibitors in Lung Adenocarcinoma Cell Models by Cotargeting the MAPK Pathway or HSP90

Liu

Lü

et al. 2021

Journal of Oncology

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Background. KRASG12C inhibitors have shown promising efficacy in early clinical trials, but drug resistance compromises their long-term benefits. Therefore, it is critical to understand the mechanisms of drug resistance and to design appropriate combinatory treatments to improve efficacy. Methods. To understand the comprehensive mechanisms of drug resistance, we treated lung cancer cells with KRASG12C inhibitors for different periods and performed transcriptional profiling and signaling analysis to identify critical factors and pathways that drive drug tolerance and resistance. We also evaluated several drug combinations in vitro and in vivo to identify potentially effective therapeutics. Results. We found that the feedback activation of multiple receptor tyrosine kinases (RTKs) may have cooperatively induced intrinsic and adaptive resistance to KRASG12C inhibitors. Notably, continuous KRAS inhibition induced a multidrug-resistant phenotype, implying that upfront combinatory treatment might be required to treat this group of patients. We also demonstrated that concurrently targeting multiple nodes in the RTK/RAS/RAF/MEK/ERK axis improved the efficacy of KRASG12C inhibitors, mainly by suppressing the reactivation of the mitogen-activated protein kinase (MAPK) pathway. Moreover, the combined use of HSP90 and KRASG12C inhibitors effectively induced tumor regression in lung adenocarcinoma models in vitro and in vivo. Conclusion. Together, our findings revealed mechanisms underlying KRASG12C inhibitors resistance and provided novel candidate combinatory strategies to improve their anticancer activity.

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“…These results revealed that FER1L4 regulated the expression of PTEN protein and thus inhibited the expression of AKT phosphorylation. (17,18). We previously revealed that overexpressed FER1L4 regulated the PTEN protein and inhibited the phosphorylation of the AKT protein, which may also be related to apoptosis.…”

Section: Overexpression Of Lncrna Fer1l4 Inhibits the Invasion And Mi...mentioning

confidence: 99%

Long non‑coding RNA FER1L4 inhibits cell proliferation and promotes cell apoptosis via the PTEN/AKT/p53 signaling pathway in lung cancer

et al. 2020

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Long non-coding RNA Fer-1-like protein 4 (FER1L4) has been reported to play crucial regulatory roles in tumor progression and apoptosis. However, its clinical significance and biological role in non-small cell lung cancer (NSCLC) are completely unknown. The purpose of this study was to investigate the expression of lncRNA FER1L4 in plasma and tissues of patients with NSCLC and study the mechanism of proliferation and apoptosis of lung cancer cells. The expression levels of FER1L4 in plasma and tissues of NSCLC patients and cell lines were analyzed via RT-qPCR. The effects of FER1L4 on cell proliferation, migration and invasion were analyzed by CCK-8, wound healing and Transwell assays, respectively. The expression levels of related proteins were detected by western blot assay, while cell apoptosis was determined by Hoechst staining and flow cytometry. The results revealed that FER1L4 was significantly downregulated in NSCLC plasma and tissues and lung cancer cell lines compared to corresponding controls. Moreover, a significant decrease of cell proliferation, migration and invasion were observed in FER1L4-overexpressed cells. FER1L4 could promote phosphatase and tension homolog deleted on chromosome ten (PTEN) and p53 expression, inhibit AKT phosphorylation expression, thus increasing the proportion of apoptotic cells. The present study indicated that FER1L4 may inhibit cell proliferation and promote apoptosis of NSCLC cells via the PTEN/AKT/p53 pathway, which provides a better understanding of the pathogenesis of NSCLC and may provide a novel potential therapeutic target for clinical treatment.

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The HSP90/Akt pathway may mediate artemether‐induced apoptosis of Cal27 cells

Cited by 8 publications

References 34 publications

Artemisinin suppressed tumour growth and induced vascular normalisation in oral squamous cell carcinoma via inhibition of macrophage migration inhibitory factor

Artemisinin suppressed tumour growth and induced vascular normalisation in oral squamous cell carcinoma via inhibition of macrophage migration inhibitory factor

Enhancing the Therapeutic Efficacy of KRASG12C Inhibitors in Lung Adenocarcinoma Cell Models by Cotargeting the MAPK Pathway or HSP90

Long non‑coding RNA FER1L4 inhibits cell proliferation and promotes cell apoptosis via the PTEN/AKT/p53 signaling pathway in lung cancer

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