Sclareol ameliorated ERCC1-mediated cisplatin resistance in A549 human lung adenocarcinoma cells and a murine xenograft tumor model by suppressing AKT-GSK3β-AP1/Snail and JNK-AP1 pathways

Pan, Chun Hsu; Chen, Shih Yin; Wang, Jie Yu; Tsao, Shu Ping; Huang, Hui Yu; Chiu, Philip Wei-Chen; Wu, Chieh Hsi

doi:10.1016/j.cbi.2020.109304

Cited by 13 publications

(11 citation statements)

References 36 publications

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“…ERCC1 is one of the key regulatory proteins within the NER pathway that plays a significant role in the repair of DNA adducts and intrastrand crosslinks (ICLs) generated by cisplatin [ 79 ]. ERCC1 overexpression is found in many different types of cisplatin-resistant cancers, such as HNSCC, bladder, and lung cancers [ 19 , 80 , 81 ]. This makes ERCC1 an important predictive marker for cisplatin treatment.…”

Section: Predictive Markers Of Cisplatin Resistancementioning

confidence: 99%

Targeting DNA Damage Response and Repair to Enhance Therapeutic Index in Cisplatin-Based Cancer Treatment

Kiss

Xia

Acklin

2021

IJMS

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Platinum-based chemotherapies, such as cisplatin, play a large role in cancer treatment. The development of resistance and treatment toxicity creates substantial barriers to disease control, yet. To enhance the therapeutic index of cisplatin-based chemotherapy, it is imperative to circumvent resistance and toxicity while optimizing tumor sensitization. One of the primary mechanisms by which cancer cells develop resistance to cisplatin is through upregulation of DNA repair pathways. In this review, we discuss the DNA damage response in the context of cisplatin-induced DNA damage. We describe the proteins involved in the pathways and their roles in resistance development. Common biomarkers for cisplatin resistance and their utilization to improve patient risk stratification and treatment personalization are addressed. Finally, we discuss some of the current treatments and future strategies to circumvent the development of cisplatin resistance.

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Section: Predictive Markers Of Cisplatin Resistancementioning

confidence: 99%

Targeting DNA Damage Response and Repair to Enhance Therapeutic Index in Cisplatin-Based Cancer Treatment

Kiss

Xia

Acklin

2021

IJMS

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“…We also showed that ovarian tumours with high Polβ expression have poor survival compared to low Polβ expressing tumours. Moreover, we [83] and others [84][85][86] have demonstrated that ERCC1 is a key predictor of cisplatin resistance in ovarian, testicular and lung cancers. Depletion of ERCC1 substantially increased platinum sensitivity in the cell line model [87].…”

Section: Brca Mutations and Cisplatin Sensitivitymentioning

confidence: 74%

Can Cisplatin Therapy Be Improved? Pathways That Can Be Targeted

Ali

Aouida

Sulaiman

et al. 2022

IJMS

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Cisplatin (cis-diamminedichloroplatinum (II)) is the oldest known chemotherapeutic agent. Since the identification of its anti-tumour activity, it earned a remarkable place as a treatment of choice for several cancer types. It remains effective against testicular, bladder, lung, head and neck, ovarian, and other cancers. Cisplatin treatment triggers different cellular responses. However, it exerts its cytotoxic effects by generating inter-strand and intra-strand crosslinks in DNA. Tumour cells often develop tolerance mechanisms by effectively repairing cisplatin-induced DNA lesions or tolerate the damage by adopting translesion DNA synthesis. Cisplatin-associated nephrotoxicity is also a huge challenge for effective therapy. Several preclinical and clinical studies attempted to understand the major limitations associated with cisplatin therapy, and so far, there is no definitive solution. As such, a more comprehensive molecular and genetic profiling of patients is needed to identify those individuals that can benefit from platinum therapy. Additionally, the treatment regimen can be improved by combining cisplatin with certain molecular targeted therapies to achieve a balance between tumour toxicity and tolerance mechanisms. In this review, we discuss the importance of various biological processes that contribute to the resistance of cisplatin and its derivatives. We aim to highlight the processes that can be modulated to suppress cisplatin resistance and provide an insight into the role of uptake transporters in enhancing drug efficacy.

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“…Immunoblotting was performed following the procedure reported in our previous study with a minor modification [ 22 ]. In brief, harvested cells were lysed using the PRO-PREP Protein Extraction Solution with proteinase inhibitor cocktail (#4693159001, cOmplete, Roche) and phosphatase inhibitor cocktail (#04906837001, PhosSTOP, Roche).…”

Section: Methodsmentioning

confidence: 99%

Preventive Effect and Mechanism of Crossostephium chinense Extract on Balloon Angioplasty-Induced Neointimal Hyperplasia

Pan

Lin

Wang

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Balloon angioplasty-induced neointimal hyperplasia remains a clinical problem that must be resolved. The bioactivities of the Crossostephium chinense extract (CCE) have demonstrated potential in preventing the progression of restenosis. The present study evaluated whether CCE can suppress balloon angioplasty-induced neointima formation and elucidated its possible pharmacological mechanisms. A rat model of carotid arterial balloon angioplasty was established to evaluate the inhibitory effect of CCEs on neointimal hyperplasia. Two cell lines, A10 vascular smooth muscle cells (VSMCs) and RAW264.7 macrophages, were used to investigate the potential regulatory activities and pharmacological mechanisms of CCEs in cell proliferation and migration and in inflammation. Our in vitro results indicated that CCE3, the ethanolic extract of C. chinense, exerted the strongest growth inhibitory and antimigratory effects on VSMCs. CCE3 blocked the activation of focal adhesion kinase, platelet-derived growth factor receptor-β (PDGFRB), and its downstream molecules (AKT and mTOR) and reduced the expression of matrix metalloproteinase-2. In addition, our findings revealed that CCE3 significantly increased the expression of miRNA-132, an inhibitory regulator of inflammation and restenosis, and suppressed the expression of inflammation-related molecules (inducible nitric oxide synthase, cyclooxygenase-2, interleukin- (IL-) 1β, and IL-6). Our in vivo study results indicated that balloon injury-induced neointimal hyperplasia was inhibited by CCE3. CCE3 could reduce neointima formation in balloon-injured arteries, and this effect may be partially attributed to the CCE3-induced suppression of PDGFRB-mediated downstream pathways and inflammation-related molecules.

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Sclareol ameliorated ERCC1-mediated cisplatin resistance in A549 human lung adenocarcinoma cells and a murine xenograft tumor model by suppressing AKT-GSK3β-AP1/Snail and JNK-AP1 pathways

Cited by 13 publications

References 36 publications

Targeting DNA Damage Response and Repair to Enhance Therapeutic Index in Cisplatin-Based Cancer Treatment

Targeting DNA Damage Response and Repair to Enhance Therapeutic Index in Cisplatin-Based Cancer Treatment

Can Cisplatin Therapy Be Improved? Pathways That Can Be Targeted

Preventive Effect and Mechanism of Crossostephium chinense Extract on Balloon Angioplasty-Induced Neointimal Hyperplasia

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