MOLECULAR AND CELLULAR BIOCHEMISTRY
·
2020
·Vol. 476
·期 2
·1075-1082
·
IF 2.795
Zhang Xiaowei,Dong Yu,Gao Miao,Hao Minfeng,Ren Hui,Guo Ling,Guo Hua
The tumor necrosis factor receptor-associated protein 1 (TRAP1) is associated with the occurrence and development of various diseases, including inflammation and cancer. However, the role and mechanism of TRAP1 in the development of lung cancer need to be further explored. Therefore, the purpose of this study is to investigate the role of TRAP1 in the regulation of apoptosis by cisplatin and its special mechanism. The RT-qPCR and Western blot were used to detect the mRNA and protein expression of ANGPTL4 in A549 and H1299 cells, respectively. And the cell apoptosis and cell cycle were measured by flow cytometry (FCM). The expression of genes related to apoptosis and drug resistance as well as the cell cycle regulators, including MDM2, CyclinB1, and CDK1, were detected by Western blot. Finally, the reactive oxygen species (ROS) indicator DCFH-DA was performed to detect the generation of ROS, and the mitochondrial membrane potential (ΔΨm) was detected by JC-1 staining. The results showed that the expression of TRAP1 was significantly increased in A549/DDP and H1299/DDP than A549 and H1299 cells. Further research found that knockdown of TRAP1 induced apoptosis and caused G2/M cell cycle arrest in A549/DDP and H1299/DDP cells. What is more, siTRAP1 reduced the relative JC-1 polymer monomer fluorescence ratio and decreased the ΔΨm, up-regulated the expression of Cytochrome C. Importantly, siTRAP1 induces ROS-dependent mitochondrial dysfunction. It is suggested that that TRAP1 suppresses cisplatin-induced apoptosis by promoting ROS-dependent mitochondrial dysfunction.
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高影响因子
MOLECULES
·
2023
·Vol. 28
·期 22
·7582
·
IF 4.6
Zhiguang Zhang,Boya Liang,Wugemo Jike,Runtian Li,Xinxin Su,Jie Yu,Tongxiang Liu
Cisplatin (Cis) is considered to be one of the most effective drugs for killing cancer cells and remains a first-line chemotherapeutic agent. However, Cis’s multiple toxicities (especially nephrotoxicity) have limited its clinical use.Marsdenia tenacissima(Roxb.) Wight et Arn. (MT), a traditional Chinese medicine (TCM) employed extensively in China, not only enhances the antitumor effect in combination with Cis, but is also used for its detoxifying effect, as it reduces the toxic side effects of chemotherapy drugs. The aim of this study was to explore the therapeutic effect of MT on Cis-induced nephrotoxicity, along with its underlying mechanisms. In this study, liquid–mass spectrometry was performed to identify the complex composition of the extracts of MT. In addition, we measured the renal function, antioxidant enzymes, and inflammatory cytokines in mice with Cis-induced nephrotoxicity and conducted renal histology evaluations to assess renal injury. The expressions of the proteins related to antioxidant, anti-inflammatory, and apoptotic markers in renal tissues was detected by Western blotting (WB). MT treatment improved the renal function, decreased the mRNA expression of the inflammatory factors, and increased the antioxidant enzyme activity in mice. A better renal histology was observed after MT treatment. Further, MT inhibited the expression of the phospho-NFκB p65 protein/NFκB p65 protein (p-p65)/p65, phospho-inhibitor of nuclear factor kappa B kinase beta subunit/inhibitor of nuclear factor kappa B kinase beta subunit (p-IKKβ/IKKβ), Bcl-2-associated X (Bax), and Cleaved Caspase 3/Caspase 3 proteins, while the expression of nuclear factor-erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), Recombinant NADH Dehydrogenase, Quinone 1 (NQO1), and B-cell lymphoma-2 (Bcl-2) was increased. The present study showed that MT ameliorated renal injury, which mainly occurs through the regulation of the Nrf2 pathway, the NF-κB pathway, and the suppression of renal tissue apoptosis. It also suggests that MT can be used as an adjuvant to mitigate the nephrotoxicity of Cis chemotherapy.Keywords:Marsdenia tenacissima;cisplatin;nephrotoxicity;oxidative stress;inflammation;apoptosis
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Acta Pharmaceutica Sinica B
·
2024
·
IF 14.7
Hua-yang Fan,Ming-da Zhao,Hong-jie Jiang,Zhen-wei Yu,Yu-jiang Fan,Xin-hua Liang,Ya-ling Tang,Yong Sun
Circular RNAs (circRNAs) are ideal biomarkers of oral squamous cell carcinoma (OSCC) because of their highly stable closed-loop structure, and they can act as microRNA (miRNA) sponges to regulate OSCC progression. By analyzing clinical samples, we identified circCPNE1, a dysregulated circRNA in OSCC, and its expression level was negatively correlated with the clinical stage of OSCC patients. Gain-of-function assays revealed the tumor-suppressive effect of circCPNE1, which was then identified as a miR-330-3p sponge. MiR-330-3p was recognized as a tumor promoter in multiple studies, consistent with our finding that it could promote the proliferation, migration, and invasion of OSCC cells. These results indicated that selective inhibition of miR-330-3p could be an effective strategy to inhibit OSCC progression. Therefore, we designed cationic polylysine-cisplatin prodrugs to deliver antagomiR-330-3p (a miRNA inhibitory analog) via electrostatic interactions to form PP@miR nanoparticles (NPs). Paratumoral administration results revealed that PP@miR NPs effectively inhibited subcutaneous tumor progression and achieved partial tumor elimination (2/5), which confirmed the critical role of miR-330-3p in OSCC development. These findings provide a new perspective for the development of OSCC treatments.
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INTERNATIONAL JOURNAL OF PHARMACEUTICS
·
2024
·
IF 5.3
Yanyan Zhang,Gareth R. Williams,Tong Wang,Yilu Zheng,Jianxiang Xu,Van Cuong Nguyen,Lili Yao,Haijun Wang,Li-Min Zhu
A multifunctional nanoplatform was constructed in this work, with the goal of ameliorating the challenges faced with traditional cancer chemotherapy. Cisplatin (CP) was loaded into mesoporous polydopamine (mPDA) nanoparticles (NPs) with a drug loading of 15.8 ± 0.1 %, and MnO 2 used as pore sealing agent. Finally, the NPs were wrapped with platelet membrane (PLTM). P-selectin on the PLTM can bind to CD44, which is highly expressed on the tumor cell membrane, so as to improve the targeting performance of the NPs. In addition, the CD47 on the PLTM can prevent the NPs from being phagocytosed by macrophages, which is conducive to immune escape. The final PLTM-CP@mPDA/MnO 2 NPs were found to have a particle size of approximately 198 nm. MnO 2 is degraded into Mn 2+ in the tumor microenvironment, leading to CP release from the pores in the mPDA. CP both acts as a chemotherapy agent and can also increase the concentration of H 2 O 2 in cells. Mn 2+ can catalyze the conversion of H 2 O 2 to OH, resulting in oxidative damage and chemodynamic therapy. In addition, Mn 2+ can be used as a contrast agent in magnetic resonance imaging (MRI). In vitro and in vivo experiments were performed to explore the therapeutic effect of the NPs. When the concentration of CP is 30 μg/mL, the NPs cause approximately 50 % cell death. It was found that the PLTM-CP@mPDA/MnO 2 NPs are targeted to cancerous cells, and in the tumor site cause extensive apoptosis. Tumor growth is thereby repressed. No negative off-target side effects were noted. MRI could be used to confirm the presence of the NPs in the tumor site. Overall, the nano-platform developed here provides cooperative chemotherapy and chemodynamic therapy, and can potentially be used for effective cancer treatment which could be monitored by MRI.
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Polymer Chemistry
·
2024
·Vol. 15
·期 28
·2883-2898
·
IF 4.1
Yaodong Di,Hanning Zhang,Zimu Luo,Congshu Feng,Xi Zhang,Shuai Yang,Jie Hou,Lesan Yan
In tumor treatment, traditional single therapies such as chemotherapy or photothermal therapy often suppress tumor growth while also causing serious toxic side effects on normal tissues and organs. Additionally, reducing drug dosage is challenging to achieve the desired therapeutic effects. Therefore, combining chemotherapy and photothermal therapy has become an effective strategy to enhance tumor treatment efficiency. To achieve this, a biodegradable amphiphilic block copolymer with carboxyl-functionalized side chains, named mPEG-b-P(CL-co-MPC/TMA), was designed and synthesized. It was then complexed with cisplatin to successfully prepare mPEG-b-P(CL-co-MPC/TMA)-Pt. Subsequently, the novel conjugated polymer photothermal agent PDPPDTP was encapsulated to prepare PDPPDTP-loaded mPEG-b-P(CL-co-MPC/TMA)-Pt nanomicelles. These nanomicelles not only co-deliver cisplatin drugs and photothermal agents but also exhibit excellent stability and photothermal performance. Under lower doses of cisplatin drugs and photothermal effects, they can still efficiently eradicate tumor cells in a relatively gentle manner, demonstrating significant potential in synergistic cancer therapy.
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JOURNAL OF COLLOID AND INTERFACE SCIENCE
·
2025
·
IF 9.7
Weijie Zhang,Xiaofei Wang,Peng Wang,Qingdong Li,Yankun Zhang,Xiaoshuo Meng,Geng Tian,Jianmin Xiao,Guilong Zhang
Cisplatin (CDDP), a first-line chemotherapeutic agent, faces significant challenges in the treatment of non-small-cell lung cancer (NSCLC) due to the rapid emergence of drug resistance. In this study, a glucose transporter protein 1-targeted nanodrug (RCPM) was developed by coordinating rutin with polymetallic ions, including Fe, V , and Pt. RCPM selectively targeted CDDP-resistant A549 (A549R) cells, efficiently accumulating within tumors. Exhibiting exceptional photothermal (PT) properties, RCPM facilitated PT-induced tumor ablation. Within the tumor microenvironment, RCPM underwent degradation, releasing high concentrations of V , Fe, and CDDP. The liberated V and Fe ions catalyzed the Fenton reaction, generating reactive oxygen species (ROS) and inducing ferroptosis. Simultaneously, these metal ions synergistically suppressed the expression of excision repair cross-complementing 1 (ERCC1), glutathione (GSH), and adenosine triphosphate (ATP), effectively disrupting DNA repair pathways, preventing CDDP inactivation, and enhancing its cytotoxicity against A549R tumors. Furthermore, RCPM demonstrated complete and rapid renal clearance, ensuring excellent biosafety and strong clinical translational potential. In vivo studies revealed that a single administration of RCPM, combined with PT therapy, significantly inhibited NSCLC progression. These findings highlight RCPM as a promising nanodrug for overcoming CDDP resistance and enhancing NSCLC treatment efficacy.
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BIOCHEMICAL PHARMACOLOGY
·
2025
·
IF 5.6
Qihang Guo,Yue Mao,Jiyu Zhang,Yangyang Zhou,Yue Zhao,Ying Li,Jinglong Lv,Huiyu Yang,Bingrong Liu
Esophageal cancer, a malignant neoplasm originating from the epithelial cells of the esophagus, predominantly manifests as esophageal squamous cell carcinoma (ESCC) in approximately 90% of cases in China. Cisplatin-based chemotherapy regimens remain the first-line therapeutic option for ESCC, however, the five-year overall survival rate of patients is disappointingly low. Oridonin, a bioactive diterpenoid extracted from the traditional Chinese medicine herb Donglingcao, has demonstrated inhibitory effects against various malignancies. Currently, research on the combination of oridonin and cisplatin for the treatment of ESCC is limited. This study aims to elucidate the potential synergistic anti-cancer effects of oridonin in combination with cisplatin on ESCC, along with the underlying synergistic molecular mechanisms. In vitro experiments revealed that the combination of oridonin and cisplatin could synergistically inhibit ESCC cell proliferation, migration, invasion. The synergistic effect also induced cell cycle arrest and promoted apoptosis via the mitochondrial pathway by augmenting NOXA transcriptional activity and activating the NOXA-BCL2 axis. In vivo experiments corroborated these findings, showing a marked reduction in the growth of subcutaneous xenograft tumors in mice treated with the combination, without exacerbating the cisplatin-associated side effects such as weight loss or hepatic and renal toxicity. In conclusion, the combination of oridonin and cisplatin can synergistically inhibit the development of ESCC through the activation of the NOXA-BCL2 axis signaling pathway. This treatment is both safe and effective, presenting a promising prospect for combined therapeutic application in ESCC management.
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Acta Pharmaceutica Sinica B
·
2020
·
IF 7.097
Yanjuan Huang,Zhanghong Xiao,Zilin Guan,Zishan Zeng,Yifeng Shen,Xiaoyu Xu,Chunshun Zhao
The “vicious cycle” established between tumor growth and osteolysis aggravates the process of breast cancer bone metastasis, leading to life-threatening skeletal-related events that severely reduce survival and quality of life. To effectively interrupt the “vicious cycle”, innovative therapeutic strategies that not only reduce osteolysis but also relieve tumor burden are urgently needed. Herein, a bone-seeking moiety, alendronate (ALN), functionalized coordination polymer nanoparticles ( [email protected] ) co-delivering cisplatin prodrug (DSP) and antiresorptive agent zoledronate (ZOL) via Zn 2+ crosslinking for combination therapy was reported. The versatile [email protected] with a diameter of about 40 nm can cross the fissure in the bone marrow sinus capillaries, and possesses an excellent bone-seeking ability both in vitro and in vivo . Additionally, [email protected] could synergistically inhibit the proliferation of cancer cells, suppress the formation of osteoclast-like cells and induce the apoptosis of osteoclasts in vitro . Importantly, it could preferentially accumulate in bone affected site, remarkably inhibit the proliferation of tumor cells, relieving bone pain, and significantly inhibit the activation of osteoclasts, protecting the bone from destruction in vivo , eventually leading to the breakdown of “vicious cycle” without inducing obvious systemic toxicity. This innovative nanoagent combines chemotherapy and osteolysis inhibition, exhibiting an inspiring strategy for effective treatment of bone metastasis.
研究领域:
肿瘤学
·
药学
·
纳米技术
·
生物材料
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JOURNAL OF ETHNOPHARMACOLOGY
·
2026
·
IF 6.8
Fuyu Xiong,Yuxin Bai,Shifei Wu,Yulu Wang,Xinjie Dai,Yang Yang,Jiyu Gong,Gaole Zhang,Tianzhu Zhang
Ethnopharmacological relevance Yupingfeng San (YPFS), a classic tonic formula in Traditional Chinese Medicine (TCM), has been extensively applied clinically for centuries. Originating from Jiuyuan Fang , its earliest extant record is Danxi Xinfa . YPFS is composed of Huangqi ( Astragalus membranaceus Bunge), Baizhu ( Atractylodes rubra Dekker), and Fangfeng ( Saposhnikovia divaricata (Turcz.) Schischk). Due to its traditional efficacy of " replenishing qi and consolidating the exterior," YPFS is commonly prescribed for allergic rhinitis, nephrotic syndrome, and chronic nephritis. Recent studies have confirmed that YPFS protects renal function and alleviates renal fibrosis in mice with diabetic nephropathy, while simultaneously improving lung function and reducing pulmonary fibrosis in bleomycin-induced rats. Taken together, these results suggest YPFS possesses substantial potential for mitigating organ fibrosis. Purpose This study investigated the renoprotective efficacy and underlying mechanism of YPFS extract in a cisplatin-induced mouse model of renal interstitial fibrosis. Using an integrated in vivo and in vitro approach, we sought to validate the therapeutic potential of this traditional formula against chemotherapy-induced nephrotoxicity. Methods The chemical components of YPFS extract were analyzed using UPLC-Q-TOF -MS. For the in vivo study, male BALB/c mice received YPFS extract (1, 1.95, or 3 g/kg) by oral administration once daily for 7 days after a single injection of cisplatin (20 mg/kg, i.p.). Renal function was assessed by measuring serum creatinine, plasma BUN, fasting blood glucose, and the urine protein-to-creatinine ratio. Kidney tissues were examined using H&E and Masson's trichrome staining for histopathological analysis, and the expression of fibrosis markers (α-SMA, collagen I, fibronectin) was measured by immunohistochemistry and western blotting. For the in vitro study, MPC-5 podocytes were treated with high glucose (25 mM) for 48 h to induce injury, and then intervened with YPFS extract at concentrations of 20, 40, or 80 μg/mL, along with JAK2 inhibitor AG490 and STAT3 agonist Colivelin for mechanism verification. Cell viability was measured by MTT assay, apoptosis was assessed by Hoechst 33342 staining, the expression of α-SMA was measured by cellular immunofluorescence, and mitochondrial morphology was observed using MitoTracker Red staining and TEM. Mitochondrial function was evaluated by Na + /K + -ATPase and Complex I activities, and oxidative stress levels were determined by T-SOD, GSH, and MDA assays. RNA-seq was conducted to identify DEGs in MPC-5 cells, and Western blotting was used to verify key protein expression in both cells and tissues. Results UPLC-Q-TOF-MS analysis identified 57 compounds in YPFS extract, predominantly flavonoids (40.35%) and saponins (21.05%). In cisplatin-treated mice, the extract dose-dependently reduced serum creatinine, blood urea nitrogen, Urine protein-to-creatinine ratio, and fasting blood glucose. It also decreased collagen deposition and α-SMA overexpression in kidney tissues. In MPC-5 cells, the extract restored cell viability, reduced apoptosis and α-SMA overexpression, improved mitochondrial membrane potential and redox balance, and restored mitochondrial fusion-fission balance by increasing Mfn1/2 and decreasing Drp1 expression. Transcriptomic analysis revealed that the extract reversed the high glucose-induced activation of gene pathways related to IL-6/JAK/STAT3 signaling, oxidative phosphorylation, and apoptosis, with findings confirmed at the protein level. Mechanistic investigations using the JAK2 inhibitor AG490 and STAT3 agonist Colivelin confirmed that the cytoprotective and anti-fibrotic effects of YPFS were primarily dependent on the IL-6/JAK/STAT3 signaling pathway. Conclusion YPFS extract ameliorates cisplatin-induced renal interstitial fibrosis by suppressing IL-6/JAK/STAT3 signaling and restoring mitochondrial homeostasis. These findings provide a pharmacological basis for the traditional use of this formula and highlight its potential as an adjunct therapy for reducing chemotherapy-related kidney injury.
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International Journal of Pharmaceutics-X
·
2025
·
IF 6.4
Yinghan Wang,Shichao Liu,Feikai Zhu,Xuefei Wang,Hanyu Wang,Lin Long,Jun Xiao,Chuanlong Guo
Acute kidney injury (AKI) is a common and serious complication in clinical practice, especially when using chemotherapy drug cisplatin, which severely limits its anti-cancer efficacy. This study developed a novel nano delivery system (Fu-4-PBA/Po NPs) that combines fucoidan (Fu), endoplasmic reticulum stress (ERS) inhibitor 4-phenylbutyric acid (4-PBA), and natural antioxidant Polydatin (Po) to simultaneously alleviate cisplatin induced oxidative stress and ERS. The optimized Fu-4-PBA/Po NPs showed an average size of 102 ± 3.46 nm, a zeta potential of −16.5 ± 0.49 mV, and a high drug loading capacity of 10.34 ± 0.6 %. They exhibited excellent stability and a sustained release profile in vitro . In vitro results showed that treatment with Fu-4-PBA/Po NPs led to a marked increase in cell survival by 34.73 ± 3.54 percentage points compared to the model group, which had a survival rate of 45.97 ± 2.76 %. Furthermore, Fu-4-PBA/Po NPs effectively inhibited the accumulation of reactive oxygen species (ROS), mitochondrial membrane potential decline, and calcium ion release by targeting P-selectin and endoplasmic reticulum (ER) at the site of inflammation, and significantly alleviate cisplatin induced cell apoptosis. Mechanism studies showed that nanocomposites alleviate ERS by inhibiting the PERK-eIF2α-ATF4-CHOP pathway, while blocking the activation of the cGAS-STING pathway, thereby reducing DNA damage and inflammatory response. Pharmacokinetic studies showed that the peak concentration (Cmax) of the nanoparticles reached 2.2 times that of free Po, and the area under the curve (AUC) increased by 2 times. In animal studies, administration of Fu-4-PBA/Po NPs at a dose of 100 mg/kg notably ameliorated renal function, as indicated by reductions in serum creatinine (SCr) and blood urea nitrogen (BUN) levels by 84.3 % and 62.4 %, respectively, and also improved kidney histopathology. This study provided a dual targeted nano-delivery strategy for cisplatin induced AKI therapy, which has important clinical application potential.
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INTERNATIONAL JOURNAL OF HYPERTHERMIA
·
2024
·
IF 3
Guanghui Zi,Jin Chen,Yatu Peng,Yue Wang,Baowei Peng
Background Hyperthermia can play a synergistic role with chemotherapy in combination therapy. Although the association between caspase activation, apoptosis, and pyroptosis have been published for both cisplatin (CDDP) and hyperthermia therapies independently, the interactions between these molecular pathways in combination therapy are unknown. The present study aimed to investigate the possible interactions between caspase 8 activation, apoptosis, and pyroptosis in combination therapy.Methods Cells were treated with CDDP (15 µg/ml), followed by hyperthermia at optimized temperature (42.5 °C) in water-bath. After combination therapy, cell viability was analyzed by CCK-8, and cell death was analyzed by Annexin-V-FITC/PI and caspases activation. Immuno-staining and co-immuno-precipitation were used to examine the interaction between p62 and caspase-8. Pyroptosis was investigated by western blotting and transmission electron microscopy. E3 ligase Cullin 3 was knockdown by siRNA. In addition, caspase-8 activation was modulated by CRISPR-Cas9 gene-editing or pharmacological inhibition.Results Combination therapy promoted K63-linked polyubiquitination of caspase-8 and cellular accumulation of caspase-8. In turn, polyubiquitinated caspase-8 interacted with p62 and led to the activation of caspase-3. Knockdown of the E3 ligase Cullin 3 by siRNA reduced caspase-8 polyubiquitination and activation. In addition, combination therapy induced release of the pore-forming N-terminus from gasdermins and promoted pyroptosis along with caspase-8 accumulation and activation. Knockdown of caspase-8 by CRISPR/Cas9 based gene editing reduced the sensitivity of tumor cells to apoptosis and pyroptosis.Conclusions Our study presented a novel mechanism in which hyperthermia synergized with chemotherapy in promoting apoptosis and pyroptosis in a caspase-8 dependent manner.
研究领域:
肿瘤学
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分子生物学
·
细胞生物学
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Pharmaceuticals
·
2022
·Vol. 15
·期 4
·480
·
IF 5.215
Yang Qu,Zhiqi Wang,Miao Sun,Tian Zhao,Xuanlei Zhu,Xiaoli Deng,Man Zhang,Ying Xu,Hongfei Liu
Although polymeric platinum(IV) (Pt(IV)) prodrugs can reduce the side effects of cisplatin, the efficacy of the prodrug is still limited by its non-targeted distribution, poor penetration in deep tumor tissue, and low cytotoxicity in tumor cells. To improve the clinical potential of polymeric prodrug micelle, we synthesized amphiphilic polymeric Pt(IV) with high Pt content (22.5%), then developed a theranostic nanocomplex by integrating polymeric Pt(IV) with superparamagnetic Mn0.6Zn0.4Fe2O4via simple self-assembly. Due to the high content of Mn0.6Zn0.4Fe2O4(41.7%w/w), the theranostic nanocomplex showed high saturation magnetization (103.1 emu g−1) and excellent magnetocaloric effect (404 W g−1), both of them indicating its advantages in efficient magnetic targeting (MT), magnetic hyperthermia (MH), and magnetic resonance imaging (MRI). In vitro, in combination with MH, the theranostic nanocomplex showed as high cytotoxicity as cisplatin because of a significant increase in platinum of cellular uptake. In vivo, the accumulation of theranostic nanocomplex in tumors was increased by MT and confirmed by MRI. Furthermore, MH improved penetration of theranostic nanocomplex in tumors as expanding blackened area in tumors was observed by MRI. Based on these properties, the theranostic nanocomplex, under the assistance of MT and MH, showed the highest tumor growth inhibition rate (88.38%) after different treatments, while the body weight of mice increased slightly, indicating low side effects compared to those of cisplatin. The study provided an advanced theranostic nanocomplex with low toxicity and high efficacy, indicating a great clinical potential of polymeric Pt(IV).Keywords:polymeric prodrug;theranostic nanocomplex;pH-triggering releasing;magnetic targeting;magnetic hyperthermia;magnetic resonance imaging
研究领域:
肿瘤学
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药剂学
·
生物医学工程
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