The concurrent treatment of Scutellaria baicalensis Georgi enhances the therapeutic efficacy of cisplatin but also attenuates chemotherapy-induced cachexia and acute kidney injury

Huang, Tse-Hung; Wu, Tsung‐Han; Guo, Yihui; Li, Tsung‐Lin; Chan, Yi-Lin; Wu, Changshan

doi:10.1016/j.jep.2019.112075

Cited by 25 publications

(21 citation statements)

References 18 publications

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“…chemotherapy in EGFR wild-type NSCLC tumors remains poor (22). Cisplatin, a commonly used chemotherapeutic, is widely used for treatment of NSCLC patients, while both its cytotoxicity and effective dose are relatively high (23). It is important to find novel therapeutic strategies to increase the efficacy of cisplatin while reducing its side effects.…”

Section: Discussionmentioning

confidence: 99%

CD44 inhibition attenuates EGFR signaling and enhances cisplatin sensitivity in human EGFR wild‑type non‑small‑cell lung cancer cells

Yin

Zhang

et al. 2020

Int J Mol Med

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cluster of differentiation 44 (cd44) as a transmembrane glycoprotein is found to be expressed in non-small cell lung cancer (NSCLC), is significantly associated with NSLC progression, metastasis and drug resistance. This study aimed to explore whether CD44 inhibition improves the sensitivity of epidermal growth factor receptor (EGFR) wild-type NSCLC cells to cisplatin and how it affects wild-type EGFR in NSCLC cells. Small interfering RNA was used to knockdown CD44 expression in EGFR wild-type NSCLC cell line H460. Results suggested that CD44 downregulation reduced cell growth, promoted G 0 /G 1 cell cycle arrest and induced cell apoptosis in H460 cells and these effects were evidently enhanced when in combination with cisplatin. Deactivation of EGFR signaling pathway including EGFR phosphorylation and its downstream molecules, targets ERK, AKT1 and SRC which were also observed in CD44-silenced H460 cells with or without EGF stimulation. Furthermore, the CD44 expression level was positively correlated with wild-type EGFR level in human lung adenocarcinoma tissues and CD44 inhibition significantly accelerated the degradation of EGFR, indicating that enhanced sensitivity of H460 cells to cisplatin by downregulation of CD44 might be due to EGFR degradation. This study demonstrated that suppression of CD44 deactivated EGFR signals in NSCLC cells with wild-type EGFR, thereby contributing to the inhibition of cell proliferation and the reinforcement of cisplatin sensitivity. It is suggested that downregulation of CD44 could be a novel potential therapeutic strategy for the treatment of EGFR wild-type NScLc.

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Section: Discussionmentioning

confidence: 99%

CD44 inhibition attenuates EGFR signaling and enhances cisplatin sensitivity in human EGFR wild‑type non‑small‑cell lung cancer cells

Yin

Zhang

et al. 2020

Int J Mol Med

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“…The standardized extract of Panax ginseng can alleviate the symptoms of cachexia induced by DDP (Lobina et al, 2014). Scutellaria baicalensis (SB) Georgi extract can not only alleviate the skeletal muscle atrophy caused by DDP but also reduce kidney damage (Huang et al, 2019). Modified Sijunzi decoction can reduce DDP-induced skeletal muscle mitochondrial dysfunction (Chen et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Linalool Prevents Cisplatin Induced Muscle Atrophy by Regulating IGF-1/Akt/FoxO Pathway

Zhang¹,

Chi

Chen

et al. 2020

Front. Pharmacol.

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Skeletal muscle atrophy is an important feature of cancer cachexia, which can be induced by chemotherapy, and affects the survival and quality of life of cancer patients seriously. No specific drugs for cancer cachexia have been applied in clinical practice. This study explored the therapeutic effect of linalool (LIN) on cisplatin (DDP) induced skeletal muscle atrophy. In vivo, LIN can improve skeletal muscle weight loss, anorexia, muscle strength decline and other cachexia symptoms caused by cisplatin treatment in a Lewis lung cancer tumor bearing mouse model, and cause no adverse effects on the anti-tumour effect. LIN treatment decreased the expression of muscle RING-finger protein-1 (MuRF1) and Atrogin1(MAFbx) in muscle, and the activation of insulin-like growth factor-1 (IGF-1)/protein kinase B (Akt)/forkhead box O (FoxO) pathway was observed. In vitro, LIN alleviated DDP induced C2C12 myotube atrophy, and IGF-1 receptor inhibitor Picropodophyllin (PIC), which had no adverse effect on C2C12 myotube cells, could reverse the protective effect of LIN. These results indicate that LIN down-regulates the expression of Atrogin1 and MuRF1 through the IGF-1/Akt/FoxO pathway, alleviating DDP-induced muscle atrophy and improving cachexia symptoms. LIN has the potential to be developed as a drug against cancer cachexia.

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“…Overexpressing of SIRT3 promoted the autophagy and reduced the inflammasomes which are assembling in kidney injury caused by sepsis (Zhao et al, 2018). The use of cisplatin is often limited by the presence of AKI during chemotherapy (Huang et al, 2019). Research shows that cisplatin may inhibit autophagy and activate NLRP3 leading to the kidney injury (Qu et al, 2018).…”

Section: Inflammasomes In Acute Kidney Injurymentioning

confidence: 99%

Role of Inflammasomes in Kidney Diseases via Both Canonical and Non-canonical Pathways

Xiang

Zhu

et al. 2020

Front. Cell Dev. Biol.

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Inflammasomes, multiprotein complex induced by harmful factors in the body, play a crucial role in innate immunity. Activation of inflammasomes lead to the activation of casepase-1 and then the secretion of inflammatory cytokines, including IL-1β and IL-18, subsequently leading to a type of cell death called pyroptosis. There are two types of signaling pathways involved in the process of inflammasome activation: the canonical and the non-canonical signaling pathway. The canonical signaling pathway is mainly dependent on casepase-1; the non-canonical signal pathway, which was recently discovered, is mainly dependent on caspase-11, but is also meditated by caspase-4, caspase-5, and caspase-8. Kidney inflammation is basically associated with inflammatory factor exudation and inflammatory cell infiltration. Several studies have showed that inflammasomes are closely related to kidney diseases, especially the NOD-, LRR-and pyrin domain-containing 3 (NLRP3) inflammasome, which play a role in regulating kidney inflammation and fibrosis. In this review, we focus on the relationship between inflammasomes and kidney diseases, especially the role of the NLRP3 inflammasome in different kinds of kidney disease via both canonical and non-canonical signal pathways.

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The concurrent treatment of Scutellaria baicalensis Georgi enhances the therapeutic efficacy of cisplatin but also attenuates chemotherapy-induced cachexia and acute kidney injury

Cited by 25 publications

References 18 publications

CD44 inhibition attenuates EGFR signaling and enhances cisplatin sensitivity in human EGFR wild‑type non‑small‑cell lung cancer cells

CD44 inhibition attenuates EGFR signaling and enhances cisplatin sensitivity in human EGFR wild‑type non‑small‑cell lung cancer cells

Linalool Prevents Cisplatin Induced Muscle Atrophy by Regulating IGF-1/Akt/FoxO Pathway

Role of Inflammasomes in Kidney Diseases via Both Canonical and Non-canonical Pathways

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