PHYTOMEDICINE
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2025
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IF 8.3
Xinyuan Jiang,Zhiyong Xu,Huan Wang,Jiangnan Zhao,Nueraili Maihemuti,Sujing Jiang,Mingshu Xiao,Kaiyue Zhang,Sibei Liang,Yueli Shi,Kai Wang
Background and purpose : As a malignant tumor characterized by a dismal prognosis and a high mortality rate, non-small cell lung cancer (NSCLC) presents significant challenges in contemporary treatment. These challenges include drug resistance and side effects, which severely hamper the effectiveness of current therapeutic strategies. An increasing number of herbal formulas have been utilized in antitumor therapy, owing to their cost-effectiveness, beneficial efficacy, and additional advantages. FuZhengXiaoJi Decoction (FZXJD), a cancer-treating formula, has been successfully applied in NSCLC clinical treatment, but the underlying mechanism remains elusive. Therefore, this paper integrated multiple analytical methods, including network pharmacology, metabolomics, biological approaches, and molecular docking to clarify how FZXJD suppresses NSCLC. Methods : This study assessed the anti-NSCLC efficacy of FZXJD using in vitro assays and lung cancer xenograft models, and the primary components and potential mechanisms of FZXJD inhibition of NSCLC were identified by high-performance liquid chromatography (HPLC) and network pharmacology. Subsequently, inhibitory mechanisms of FZXJD and its principal effector component oleanolic acid (OA) on NSCLC were explored by molecular docking, as well as biological experiments. Finally, effects of FZXJD on critical metabolic pathways in tumors were further investigated by metabolomics and metabolite enrichment analysis. Results : Inhibition of FZXJD on NSCLC cells was confirmed in vitro experiments. Correspondingly, in vivo experiments revealed that FZXJD impeded tumor progression without obvious toxic side effects. Network pharmacology and molecular docking disclosed that target genes involved in FZXJD’s inhibition of NSCLC were significantly enriched in the PI3K/AKT and ERK/MAPK signaling pathways. Additionally, 14 core genes (HSP90AA1, VEGFA, AKT1, JUN, EGFR, CASP3, ESR1, ERBB2, STAT3, MTOR, SRC, MDM2, CCND1, MAPK3) as well as the main component of the antitumor effect of FZXJD, the OA, were also identified. Biological experiments and molecular docking demonstrated that FZXJD and OA exerted antitumor effects by inhibiting two significant pathways, PI3K/AKT and ERK/MAPK. Metabolomics analysis indicated that FZXJD treatment suppressed glutathione metabolism in vivo. Conclusion FZXJD and its main active ingredient, OA, impede NSCLC progression by inhibiting PI3K/AKT and ERK/MAPK signaling pathways. FZXJD treatment also markedly attenuates glutathione metabolism. This research provides a promising strategy for the application of herbal formulas in NSCLC.
研究领域:
肿瘤学
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中药学
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生物信息学
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药理学
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产品关联
DOI
PubMed
高影响因子
CURRENT PHARMACEUTICAL DESIGN
·
2025
·Vol. 31
·期 42
·3416-3426
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IF 2.8
Chenguang Yao,Ting Tan,Jiangning Yan,Zijia Zhao,Romina Onintsoa Diarimalala,Junjie Wang,William Wang,Hanluo Li,Jingbiao Liu,Yanhong Wei,Kanghong Hu
ObjectiveTo develop new Anderson-type polyoxometalates (POMs) with high efficiency and low cytotoxicity, and investigate the effects and mechanisms against lung (A549), cervical (Hela), and breast cancer (MCF7) cell lines.MethodsCytotoxicity assessments on Hela, A549, and MCF-7 tumor cells were tested by MTT assay. Antitumor activities of B1 (vanadium-centered, methyl-modified) and B7 (vanadium-centered, hydroxyl-modified) were detected by apoptosis, scratch, and colony formation assay. The antitumor molecular mechanisms were explored by Western blotting.ResultsThis study synthesized and evaluated twelve Anderson-type compounds which were centered with vanadium, chromium, iron, cobalt, nickel, and copper heteroatoms, modified with methyl and hydroxyl at the side chains. Cytotoxicity assessments revealed that compounds B1 and B7 exhibited superior efficacy, with IC50 values of approximately 7 μmol/L of three cell lines. B1 and B7 inhibited proliferation and migration in these cell lines and induced apoptosis in MCF7 and A549 cells. Mechanistic investigations indicated that B1 induces apoptosis in MCF7 cells by inhibiting the AKT signaling pathway and downregulating the expression of apoptosis-related proteins Bcl-2 and Caspase-9.ConclusionNovel Anderson-type POMs B1 (vanadium-centered, methyl-modified) and B7 (vanadium-centered, hydroxyl-modified) exhibited superior efficacy against tumor cells and induced apoptosis via PI3K/AKT pathway, which provides new theoretical avenues for developing POM-mediated antitumor chemotherapeutic medications.
研究领域:
肿瘤学
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药理学
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分子生物学
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无机化学
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转化医学
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
Frontiers in Nutrition
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2022
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IF 6.59
Chen Lin,Jiang Qihong,Lu Hongling,Jiang Chenkai,Hu Wenjun,Yu Shaofang,Xiang Xingwei,Tan Chin Ping,Feng Yongcai,Zhang Jianfang,Li Mingqian,Shen Guoxin
Type 2 diabetes mellitus (T2DM) is a metabolic disease characterized by hyperglycemia. The aim of this work was to investigate the effect of sciadonic acid (SA) on disorders of glucolipid metabolism and intestinal flora imbalance and to further investigate its potential molecular mechanism of anti-diabetes. The experimental data indicated that SA could alleviate hyperlipidemia, insulin resistance, oxidative stress, the inflammatory response, repair liver function damage, and promote glycogen synthesis caused by T2DM. SA could also activate the PI3K/AKT/GLUT-2 signaling pathway, promote glucose metabolism gene expression, and maintain glucose homeostasis. Furthermore, 16S rRNA analysis revealed that SA could reduce the Firmicutes/Bacteroidota (F/B) ratio; promote norank_f__Muribaculaceae, Allobaculum, Akkermansia, and Eubacterium_siraeum_group proliferation; increase the levels of major short-chain fatty acids (SCFAs), such as acetic acid, propionic acid, and butyric acid; and maintain the homeostasis of the intestinal flora. In conclusion, these results suggested that SA could reshape the structural composition of intestinal microbes, activate the PI3K/AKT/GLUT2 pathway, improve insulin resistance, and decrease blood glucose levels.
研究领域:
药理学
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内分泌学
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微生物学
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代谢学
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DOI
PubMed
高影响因子
BIOORGANIC CHEMISTRY
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2021
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IF 5.275
Yingying Ma,Xiaorong Yang,Hongwei Han,Zhongling Wen,Minkai Yang,Yahan Zhang,Jiangyan Fu,Xuan Wang,Tongming Yin,Guihua Lu,Jinliang Qi,Hongyan Lin,Xiaoming Wang,Yonghua Yang
Triple-negative breast cancer (TNBC) has an unfavorable prognosis attribute to its low differentiation, rapid proliferation and high distant metastasis rate. PI3K/Akt/mTOR as an intracellular signaling pathway plays a key role in the cell proliferation, migration, invasion, metabolism and regeneration. In this work, we designed and synthesized a series of anilide (dicarboxylic acid) shikonin esters targeting PI3K/Akt/mTOR signaling pathway, and assessed their antitumor effects. Through three rounds of screening by computer-aided drug design method (CADD), we preliminarily obtained sixteen novel anilide (dicarboxylic acid) shikonin esters and identified them as excellent compounds. CCK-8 assay results demonstrated that compound M9 exhibited better antiproliferative activities against MDA-MB-231, A549 and HeLa cell lines than shikonin (SK), especially for MDA-MB-231 (M9: IC 50 = 4.52 ± 0.28 μM; SK: IC 50 = 7.62 ± 0.26 μM). Moreover, the antiproliferative activity of M9 was better than that of paclitaxel. Further pharmacological studies showed that M9 could induce apoptosis of MDA-MB-231 cells and arrest the cell cycle in G2/M phase. M9 also inhibited the migration of MDA-MB-231 cells by inhibiting Wnt/β-catenin signaling pathway. In addition, western blot results showed that M9 could inhibit cell proliferation and migration by down-regulating PI3K/Akt/mTOR signaling pathway. Finally, a three-dimensional quantitative structure–activity relationship (3D-QSAR) model was also constructed to provide a basis for further development of shikonin derivatives as potential antitumor drugs through structure–activity relationship analysis. To sum up, M9 could be a potential candidate for TNBC therapy.
研究领域:
药理学
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肿瘤学
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药物化学
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细胞生物学
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药物设计
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DOI
PubMed
高影响因子
BIOMEDICINE & PHARMACOTHERAPY
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2020
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IF 4.545
Ye Zhou,Meng Zhang,Zhilei Zhang,Yuming Jia,Chong Zhang,Li Peng
Hydrazinocurcumin (HZC), a curcumin analogue, serves as a tumor suppressor in breast cancer and lung cancer. In this study, we investigate the role and mechanism of HZC in regulating HepG2 cell apoptosis and tumorigenicity, and its synergistic effects with 5-fluorouracil (5-Fu). HepG2 cells were treated with HZC and/or 5-Fu to analyze the possible synergistic effects on cell proliferation, apoptosis and cell cycle distribution in vitro using EdU staining, Hoechst staining and flow cytometry, respectively. For mechanistic investigation we used pic, a phosphatase and tensin homolog (PTEN) inhibitor, and in other studies assessed the expression pattern of PTEN and PI3K/Akt signaling pathway-related genes. Additionally, we tested in vivo effects of HZC and 5-Fu treatment on growth of HepG2 cell tumors in nude mice. We found that HZC or 5-Fu induced apoptosis and repressed proliferation of HepG2 cells by upregulating the expression of PTEN and disrupting the PI3K/Akt signaling pathway activation. Moreover, HZC had a higher pro-apoptotic effect than 5-Fu. HZC and 5-Fu induced HepG2 cell apoptosis and inhibited their tumorigenicity in vivo . Inhibition of PTEN expression activated the PI3K/Akt signaling pathway and reversed the protective effects of HZC or 5-Fu. Thus, HZC and 5-Fu increase PTEN, which blocks the PI3K/Akt signaling pathway, ultimately inducing HepG2 cell apoptosis. Importantly, the synergistic combination of HZC and 5-Fu may present promising strategy for the treatment of HCC.
研究领域:
肿瘤学
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分子生物学
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药理学
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DOI
PubMed
高影响因子
EXPERIMENTAL CELL RESEARCH
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2021
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IF 3.905
Yiming Li,Yi He,Guanhui Chen,Ziqing Huang,Chen Yi,Xiliu Zhang,Feilong Deng,Dongsheng Yu
abstract Dental implant surgery is currently a routine therapy for the repair of missing dentition or dentition defects. Both clinical and basic research have elucidated that oxidative stress caused by the accumulation of reactive oxygen species (ROS) for various reasons impairs the process of osteointegration after dental implantation. Therefore, the osteogenic micro-environment must be ameliorated to decrease the damage caused by oxidative stress. Selenomethionine (SEMET) has been reported to play an important role in alleviating oxidative stress and accelerating cell viability and growth. However, it remains unclear whether it exerts protective effects on bone-marrow-derived mesenchymal stem cells (BMSCs) under oxidative stress. In this study, we explored the influence of selenomethionine on the viability and osteogenic differentiation of BMSCs under oxidative stress and the underlying mechanisms. Results showed that 1 μM selenomethionine was the optimum concentration for BMSCs under H 2 O 2 stimulation. H 2 O 2 -induced oxidative stress suppressed the viability and osteogenic differentiation of BMSCs, manifested by the increases in ROS production and cell apoptosis rates , and by the decrease of osteogenic differentiation-related markers. Notably, the aforementioned oxidative damage and osteogenic dysfunction induced by H 2 O 2 were rescued by selenomethionine. Furthermore, we found that the PTEN expression level was suppressed and its downstream PI3K/AKT pathway was activated by selenomethionine. However, when PTEN was stimulated, the PI3K/AKT pathway was down-regulated, and the protective effects of selenomethionine on BMSC osteogenic differentiation diminished, while the inhibition of PTEN up-regulated the protective effects of selenomethionine. Together, these results revealed that selenomethionine could attenuate H 2 O 2 -induced BMSC dysfunction through an antioxidant effect, modulated via the PTEN/PI3K/AKT pathway, suggesting that selenomethionine is a promising antioxidant candidate for reducing oxidative stress during the process of dental implant osteointegration.
研究领域:
牙科学
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干细胞生物学
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药理学
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分子生物学
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DOI
PubMed
高影响因子
MOLECULAR IMMUNOLOGY
·
2021
·
IF 4.407
Limei Ao,Han Gao,Lifen Jia,Shimin Liu,Jie Guo,Bingzhen Liu,Qiumei Dong
Matrine (Mat) is an alkaloid of tetracycline quinazine, and previous studies have demonstrated its specific effect on relieving rheumatoid arthritis (RA). However, the effect of Mat on joint synovial angiogenesis in the pathogenesis of RA has not been elucidated. In this study, body weight, joint swelling, arthritis index (AI) score, histopathological changes, immunohistochemical, and western blot- were used in collagen-induced arthritis (CIA) rats to detect pro-inflammatory factors and, - expression levels of key cytokines and proteins along the hypoxia-inducible factor (HIF)-endothelial growth factor (VEGF)-angiopoietin (Ang) axis and VEGF-phosphoinositide 3-kinase (PI3K) / protein kinase B (Akt) pathway. In vitro experiments were conducted to observe the effect of Mat on the proliferation, migration and lumen formation of RA-fibroblast-like synovial cells (FLS) and human umbilical vein endothelial cells (HUVECs). Results showed that Mat reduced the degree of paw swelling and AI score in CIA rats, joint synovial tissue proliferation, inflammatory cell infiltration, and neovascularization; moreover, it down-regulated the expression levels of inflammatory factors interleukin-1β, interferon-γ, and pro-angiogenic factors VEGF, placental growth factor, HIF-α, Ang-1, Ang-2, Tie-2, and phosphorylation-Akt in the ankle joint of CIA rats. In addition, the in vitro experiments showed that Mat inhibited the proliferation and migration of RA-FLS and inhibited the proliferation and lumen formation of HUVECs. Therefore, Mat exerts an anti-angiogenesis effect by regulating the HIF-VEGF-Ang axis and inhibiting the PI3K/Akt signaling pathway. This inhibits the pathogenesis and improve the symptoms of RA, and may be offered as a candidate drug for the treatment of RA.
研究领域:
药理学
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免疫学
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病理学
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分子生物学
✓ 已验证
DOI
PubMed
高影响因子
Journal of Ginseng Research
·
2026
·
IF 7.5
Qianru Yang,Xiaoxue Chen,Jintong Cai,Zhengwen Xie,Yuhan Nie,Jinghui Sun,He Li,Chunmei Wang
Background Ginseng - Schisandra herb pair is a classic representative one of the "combination of tonification and astringency" in traditional Chinese medicine. Ginseng tonifies lung Qi and benefits heart Qi, while Schisandra restrains the lung, nourishes the kidney, calms the mind, and soothes the spirit. When they are used in combination, one can play a tonifying role and another can serve as an astringency, with tonification but without stagnation and with astringency but without depression, so the combination can not only enhance the efficacy of replenishing Qi and nourishing Yin but also strengthen the effect of astringing and consolidating. However, the underlying mechanism and action of its combined use in the prevention and treatment of asthma remain unclear. Methods An asthma model in mice was established by using ovalbumin (OVA) combined with aluminum hydroxide (Al(OH) 3 ), so as to evaluate the anti-asthmatic effect of Ginseng - Schisandra herb pair and determine its optimal compatibility ratio. For further validation, an in vitro asthma model was developed by stimulating human bronchial epithelial cells (BEAS-2B) with interleukin-4 (IL-4) and tumor necrosis factor-α (TNF-α). The chemical profile of the herb pair extract was comprehensively analyzed by ultra-performance liquid chromatography-mass spectrometry (UPLC-MS). Potential bioactive components and anti-asthma mechanisms were predicted through network pharmacology analysis and subsequently verified by Western blot and immunofluorescence assays. Results Ginseng - Schisandra herb pair could improve the behavior of asthmatic mice, alleviate the pathological damage of lung tissue, reduce the levels of inflammatory factors in the serum of asthmatic mice and the asthma model BEAS-2B cells, increase the activity of superoxide dismutase (SOD), and decrease the levels of malondialdehyde (MDA) and reactive oxygen species (ROS). A total of 72 bioactive components were identified from the Ginseng - Schisandra herb pair extract, and the herb pair could inhibit the expression of PI3K-AKT pathway-related proteins in the lung tissue of asthmatic mice and BEAS-2B cells. Conclusion Ginseng - Schisandra herb pair can effectively alleviate the airway inflammatory response and oxidative stress injury by regulating the PI3K-AKT signaling pathway in mice to exert an anti-asthmatic effect. Among different compatibility ratios and compared with single herbs, the 2:1 ratio of the herb pair exhibits the optimal therapeutic efficacy.
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DOI
高影响因子
Materials Today Bio
·
2026
·
IF 11
Xin Sui,Ling-Feng Li,Bing-Wen Zhong,Zhan-Hua Cao,De-Feng Yang,Yuan Zhuang,Jia-Mu Ren,Tong-tong Yan,Bing Han,Zhi-Hui Liu
Mechanical tensile forces play a crucial role in modulating bone tissue behavior and the response of surrounding cells in vivo. During orthodontic tooth movement, tensile stresses within the periodontal ligament on the tension side stimulate bone deposition. Drawing inspiration from this biological process, our work introduces a strategy using mechanically active materials to enhance bone defect healing. We utilize liquid crystal elastomers (LCEs), a class of soft active materials known for excellent actuation performance. LCEs apply stable mechanical forces to target bone tissue, mimicking the traction of the periodontal ligament and actively promoting bone regeneration. By employing a sequential thiol-Michael/thiol-ene click reaction, optimizing component ratios, and utilizing low-temperature crosslinking, the driving temperature of LCE was significantly reduced to 27.3°C. This advancement eliminates limitations on its medical applications in tissue regeneration. Moreover, both in vitro and in vivo experiments confirm that LCE-induced tensile forces enhance bone regeneration. The LAMB1-ITGB4 signaling axis mediates the process via the PI3K-AKT pathway. This mechanobiological approach opens new avenues for bone defect healing and provides mechanistic insights into how mechanical tensile forces promote bone regeneration.
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DOI
PubMed
高影响因子
Chinese Medicine
·
2026
·Vol. 21
·期 1
·129
·
IF 7.4
Dong Jinwang,Cao Yang,Chen Xiujin,Xie Tao,Zhang Xiaobo,Zhao Qingpeng,Shi Cunhu,Miao Qiangqiang,Xu Zhengwei,Yan Liang,Dong Liang
Background Spinal cord injury (SCI) induces gut microbiota dysbiosis, which significantly affects recovery. Buyang Huanwu Decoction (BHD), a traditional Chinese medicine formula, has shown therapeutic effects on SCI. Although BHD is known to modulate gut microbiota, whether its benefits are mediated through the gut–spinal cord axis remains unclear. Methods A rat SCI model was established. BHD was administered orally, and fecal microbiota transplantation (FMT) from BHD-treated rats (BHD-FMT) was performed to assess neuroprotective and gut-protective effects. Behavioral testing, histology, and immunofluorescence evaluated motor recovery, inflammation, and neuroregeneration. Gut microbiota profiling was performed using 16S rDNA sequencing and metagenomics, while targeted metabolomics quantified tryptophan metabolites. Transcriptomics validated key pathways, and a microbiota–metabolite–signaling network was constructed. Results BHD significantly improved motor function, reduced spinal inflammation, and promoted neuronal survival and axonal regeneration. It restored gut function, reduced colonic inflammation, and enhanced ZO-1 and Occludin expression, which were further confirmed by FMT. BHD-FMT reshaped the gut microbiota and enriched Lactobacillus johnsonii , which correlated positively with recovery. Metabolomics showed increased tryptophan metabolites, including indole-3-lactic acid (ILA) and indole-3-propionic acid (IPA), with ILA strongly associated with functional improvement. Transcriptomic analysis and Western blot validation demonstrated that BHD-FMT activated the AhR–PI3K/Akt pathway, which was suppressed by an AhR antagonist. Conclusion BHD promotes neuroregeneration after SCI by reshaping gut microbiota and enhancing tryptophan metabolism, potentially exerting its effects through the L. johnsonii –ILA–AhR–PI3K/Akt network. These findings reveal a gut–spinal cord axis–mediated mechanism of BHD and highlight microecological targets for SCI therapy. Graphical
The alternative text for this image may have been generated using AI.
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DOI
PubMed
高影响因子
International Journal of Nanomedicine
·
2026
·
IF 8.7
Yan Yan,Ke Wang,Li Ren,Jun-jie Ma,Xing-chun Zhu,Hao-feng Ding,Jia-xin Chu,Zhi-gao Zhu,Jing-yi Xia,Yi Xia,Yuan Xu,Meng-han He,Wen-rui Wang,Cong-li Zhang
Purpose This study aims to address the issues that limit the clinical application of Dl-3-n-butylphthalide (NBP) due to its poor water solubility and low bioavailability, and to explore its therapeutic potential in renal ischemia-reperfusion (I/R) injury. We attempted to utilize layered double hydroxide (LDH) to construct a novel nano-drug delivery system to enhance the stability and efficacy of NBP, and to deeply investigate its potential mechanism of action.Methods By loading NBP onto LDH, LDHs-NBP nanocomplexes were successfully constructed. Subsequently, the effects of LDHs-NBP on renal function, tissue pathology, cell apoptosis, oxidative stress and mitochondrial function were systematically evaluated in rat renal ischemia-reperfusion injury models and HK-2 cell hypoxia/reoxygenation models. The molecular mechanism of the PI3K-AKT-Nrf2 signaling pathway was analyzed through immunohistochemistry and Western Blot.Results The experimental results show that the drug loading capacity of LDHs-NBP nanocomplexes is 24.26%. Compared with pure NBP, LDHs-NBP more effectively improve renal function in rats, reduces serum creatinine (SCr) and blood urea nitrogen (BUN), decreases inflammatory infiltration and structural damage in renal tissues, and exhibits stronger antioxidant capacity—evidenced by decreased malondialdehyde (MDA) levels and increased superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) activities. At the cellular level, LDHs-NBP significantly inhibits apoptosis and ROS production in HK-2 cells, alleviates mitochondrial dysfunction, and its protective effect is closely associated with activation of the PI3K-AKT-Nrf2 signaling pathway.Conclusion This study successfully constructed an NBP nano-complex based on LDH, and confirmed that LDHs-NBP has significant therapeutic advantages in renal ischemia-reperfusion injury. The mechanism may be related to the activation of the PI3K-AKT-Nrf2 pathway. This study provides experimental evidence for the application of LDHs-NBP in the treatment of renal ischemia-reperfusion injury, and shows a promising translational prospect and clinical value.
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DOI
PubMed
高影响因子
Stem Cell Research & Therapy
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2026
·
IF 7.8
Li Xiao-huan,Lian Fu-wei,Lv Feng,Luo Xiao-Ling,Hu Bang-li,Zhang Li-tu,Ning Shu-fang
Background Mesenchymal stem cells (MSCs)-derived exosomes present great potential as nanocarriers for targeted drug delivery. Moreover, the therapeutic efficacy of exosomes can be substantially enhanced through functional modifications and the incorporation of bioactive molecules. Methods In this study, the MSCs were cultured under two-dimensional (2D) and three-dimensional (3D) cell culture conditions. The culture supernatants were collected for isolating exosomes. The characteristics and yields of exosomes from 2D and 3D cultures were detected by nanoparticle tracking analysis (NTA), transmission electron microscopy (TEM), western blot analysis, and bicinchoninic acid (BCA) assay. Subsequently, 3D exosomes were loaded with miR-99b-5p and modified with iRGD peptide were formed into a new engineered exosome, designated as iRGD-Exo-miR-99b-5p. The effects of these engineered exosomes on the progression of colorectal cancer (CRC) were assessed through a series of in vivo and in vitro experiments. Results The 3D-cultured MSCs exhibited a higher yield of exosomes and enhanced uptake by CRC cells. Further in vitro experiments demonstrated that 3D-exosomes loaded with miR-99b-5p effectively inhibit the proliferation, invasion, migration and epithelial-mesenchymal transition (EMT) of CRC cells. Results from a xenograft tumor model indicate that iRGD-modified exosomes were significantly enriched at tumor sites. Furthermore, exosomes modified with iRGD and loaded with miR-99b-5p were employed for CRC treatment, resulting in substantial tumor growth inhibition and enhanced the chemotherapy efficacy of 5-fluorouracil (5-FU) in vivo, without inducing notable toxicity or side effects. Mechanistically, exosome-mediated delivery of miR-99b-5p downregulated FGFR3 expression, thereby inhibiting the activation of the PI3K/AKt signaling pathway and promoting ferroptosis, ultimately attenuating CRC progression. Conclusions Collectively, iRGD-modified 3D exosomes loaded with miR-99b-5p were able to specifically target tumor sites, thereby significantly suppressing CRC growth through the induction of ferroptosis via regulating the FGFR3/PI3K/AKt signaling pathway. These findings suggest that functional engineering and bioactive loading of 3D-exosomes derived from MSCs represent a promising strategy for targeted cancer therapy. Graphical
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DOI
高影响因子
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