TOXICOLOGY AND APPLIED PHARMACOLOGY
·
2018
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IF 3.616
Xuanxuan Dai,Changtian Yin,Guilong Guo,Yi Zhang,Chenguang Zhao,Jianchang Qian,Ouchen Wang,Xiaohua Zhang,Guang Liang
Triple negative breast cancer (TNBC) is an aggressive subgroup of human breast cancer. In this study, we have examined the potential of Schisandrin B (Sch B), a bioactive chemical compound found in Schisandra chinensis , against TNBC. We used MDA-MB-231, BT-549, and MDA-MB-468 TNBC cells and immunodeficient mice to study the effect of Sch B. Our results show that Sch B inhibits TNBC growth by inducing cell cycle arrest and by triggering apoptotic death. Sch B also inhibited the migration and colony formation of tumor cells, and prevented the growth of TNBC cells in mice. We found that these inhibitory activities were mediated through suppression of signal transducer and activator of transcription-3 (STAT3) phosphorylation and nuclear translocation. Taken together, our studies show that Sch B has potent anti-tumor activity against TNBC via a novel mechanism involving STAT3 inactivation.
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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高影响因子
Frontiers in Pharmacology
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2020
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IF 4.225
Cao Hui-Hui,Liu Dong-Yi,Lai Ye-Cai,Chen Yu-Yao,Yu Lin-Zhong,Shao Meng,Liu Jun-Shan
Background: Malignant melanoma is an extremely aggressive and metastatic cancer, and highly resistant to conventional therapies. Signal transducer and activator of transcription 3 (STAT3) signaling promotes melanoma development and progression, which has been validated as an effective target in melanoma treatment. Natural naphthoquinone shikonin is reported to exert anti-melanoma effects. However, the underlying mechanisms have not been fully elucidated.Purpose: This study aims to evaluate the anti-melanoma activities of shikonin and explore the involvement of STAT3 signaling in these effects.Methods: Zebrafish tumor model was established to evaluate the anti-human melanoma effects of shikonin in vivo. MTT assay and colony formation assay were employed to investigate the anti-proliferative effects of shikonin on human melanoma A375 and A2058 cells. Flow cytometry was used to analyze cell cycle distribution and apoptosis induction. Wound healing assay and Transwell chamber assay were conducted to examine the cell migratory and invasive abilities. Immunofluorescence assay was used to observe F-actin, Tubulin, and STAT3 localization. Western blotting was used to determine the expression levels of proteins associated with apoptosis and key proteins in the STAT3 signaling pathway. Immunoblotting was performed in DSS cross-linked cells to determine the homo-dimerization of STAT3. Gelatin zymography was employed to evaluate the enzymatic activity of MMP-2 and MMP-9. Transient transfection was used to overexpress STAT3 in cell models.Results: Shikonin suppressed melanoma growth in cultured cells and in zebrafish xenograft models. Shikonin induced melanoma cells apoptosis, inhibited cell migration and invasion. Mechanistic study indicated that shikonin inhibited the phosphorylation and homo-dimerization of STAT3, thus reduced its nuclear localization. Further study showed that shikonin decreased the levels of STAT3-targeted genes Mcl-1, Bcl-2, MMP-2, vimentin, and Twist, which are involved in melanoma survival, migration, and invasion. More importantly, overexpression of constitutively active STAT3 partially abolished the anti-proliferative, anti-migratory, and anti-invasive effects of shikonin.Conclusion: The anti-melanoma activity of shikonin is at least partially attributed to the inhibition on STAT3 signaling. These findings provide new insights into the anti-melanoma molecular mechanisms of shikonin, suggesting its potential in melanoma treatment.
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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细胞生物学
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动物模型
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PubMed
高影响因子
CANCER SCIENCE
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2026
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IF 4.9
Xinyu Xu,Jiayuan Wang,Meng Jiang,Ling Ouyang
Ovarian cancer is one of the most prevalent gynecologic malignancies worldwide. Dysregulated cell proliferation and angiogenesis are well-recognized to be involved in the pathogenesis of ovarian cancer. Nucleolar Protein 7 (NOL7), a novel RNA-binding protein, has been identified as a tumor suppressor and a key anti-angiogenetic factor. However, the function of NOL7 and its underlying molecular mechanisms in ovarian cancer remain unclear. In this study, we demonstrated that NOL7 expression was down-regulated in ovarian cancer tissues, and low NOL7 expression was associated with poorer prognosis in patients with ovarian cancer. Overexpression of NOL7 decreased cell viability, inhibited cell cycle entry and proliferation, and promoted apoptosis in OVCAR-3 and SKOV-3 cells. Additionally, NOL7 overexpression decreased VEGF-A level, increased TSP-1, and suppressed angiogenesis of human umbilical vein endothelial cells (HUVECs). Conversely, knockdown of NOL7 in ovarian cancer cells enhanced cell proliferation and angiogenesis, while reducing apoptosis. In vivo experiments further confirmed that NOL7 overexpression inhibited tumor growth and angiogenesis. Mechanistic studies revealed that NOL7 could bind to the 3′UTR of growth arrest and DNA damage inducible alpha (GADD45A), and overexpression of NOL7 up-regulated GADD45A expression by stabilizing GADD45A mRNA in ovarian cancer cells. The anti-cancer effects of the NOL7/GADD45A were mediated by inhibiting the phosphorylation of STAT3 at Ser727. Collectively, our findings indicate that NOL7 functions as a tumor suppressor in ovarian cancer and provide a novel therapeutic target for the treatment of ovarian cancer.
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高影响因子
BURNS
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2025
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IF 2.9
Jiaqi Wu,Guizhen Xu,Xinlu Zhou,Jun Wan,Huaiwei Liao,Cong Li,Yan Shi,Huicai Wen
Background This study investigated the pharmacological effects of asiatic acid (AA) on keloid fibroblasts (KFs) and elucidated its therapeutic mechanisms in keloid pathogenesis. Methods Primary human KFs were isolated and expanded for experimental analysis. Cell migration capacity was evaluated through cell scratch assay and Boyden chamber assay. Immunofluorescence staining was performed to quantify α-smooth muscle actin (α-SMA) expression in AA-treated KFs, while Western blot assessed collagen type I (Col-I), α-SMA, STAT3, and phosphorylated STAT3 (p-STAT3) protein levels. STAT3 activation was pharmacologically induced in KFs using Colivelin TFA (a STAT3 agonist), with subsequent evaluation of migratory behavior and protein expression profiles using parallel methodologies. Results AA treatment significantly inhibited the viability and migratory capacity of KFs, accompanied by downregulation of Col-I, α-SMA, and p-STAT3 expression. Pharmacological activation of STAT3 via Colivelin TFA partially rescued AA-induced suppression of KF migration and Col-I expression. Conclusions AA significantly modulates the migratory capacity and extracellular matrix (ECM)-related protein expression in KFs, with the STAT3 signaling pathway implicated in this regulatory mechanism. These findings indicate that the anti-fibrotic effects of AA are mediated through STAT3 signaling.
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INTERNATIONAL JOURNAL OF PHARMACEUTICS
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2026
·
IF 6
Yawen Yao,Min Zhang,Sai Xu,Guoping Wu,Xinwang Meng,Juan Li,Hua Yu
A chondroitin sulfate-functionalized GSH-responsive lipid-nanoparticle (CSD@DNLP) was developed for co-delivering doxorubicin (DOX) and nifuroxazide (NIF) in metastatic melanoma treatment. • Chondroitin sulfate-functionalization improved cellular uptake through targeting CD44-receptors and enhanced drugs release in tumor-mimic environment. • Synergistic effects were observed in tumor growth inhibition and metastasis repression through NIF-mediated STAT3 phosphorylation blockade and DOX-induced DNA damage. • CSD@DNLP demonstrated a promising strategy in metastatic melanoma. Tumor metastasis results in high mortality rate in patients with advanced melanoma. The hyperphosphorylation of signal transducer and activator of transcription 3 (STAT3) is closely associated with the proliferation and metastasis of melanoma. Here, we proposed a lipid-nanoparticle (CSD@DNLP) derived from the chondroitin sulfate (CS)-conjugated deoxycholic acid (DOCA) polymer (CS-ss-DOCA, CSD) for the co-delivery of doxorubicin (DOX) and STAT3 inhibitor nifuroxazide (NIF) in metastatic melanoma treatment. The superior affinity between CS and overexpressed CD44 receptors in B16F10 cells resulted in 3.3-fold enhancement of cellular uptake compared to free DOX. CSD@DNLP maintained structural stability in physiological conditions, while achieving 75.15% cumulative release within 48 h under a tumor-mimic concentration of glutathione (GSH, 20 mM). Synergistic effects were observed through NIF-mediated STAT3 phosphorylation blockade and DOX-induced DNA damage, resulting in 3.2-fold enhancement in apoptotic cells versus free drugs. In lung metastasis mice, CSD@DNLP suppressed metastatic nodule formation (36% of free DOX + NIF) via dual downregulation of matrix metalloproteinases-2 (MMP-2) and metalloproteinases-2 (MMP-9). This CS-functionalized GSH-responsive lipid-nanoparticle demonstrates a promising strategy in metastatic melanoma. Download: Download high-res image (162KB) Download: Download full-size image
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PHYTOMEDICINE
·
2026
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IF 11.3
Xuehui Li,Yunxiao Qiao,Xinyi Xu,Jinyu Zhu,Chuang Xie,Shan Lin,Lingfan Xu,Fuwen Yuan
Background Natural products from traditional medicinal plants represent an important source of anti-cancer agents and lead compounds for drug development. Saikosaponin D (SSD), a triterpenoid saponin isolated from Radix Bupleuri, exhibits anti-tumor activity but is limited by a narrow therapeutic window and cytotoxicity. Objective This study aimed to evaluate the anti-tumor activity of 6′'-O-acetylsaikosaponin D (6′'-O-acSSD), a naturally occurring acetylated derivative of Saikosaponin D that is identified in Radix Bupleuri , and to elucidate its underlying molecular mechanisms. Methods The anti-cancer effects of 6′'-O-acSSD were assessed using multiple cancer cell models, three-dimensional tumor spheroids, and patient-derived tumor organoids. Transcriptomic and bioinformatic analyses were performed to identify regulated cell death pathways. Molecular docking, molecular dynamics simulation, cellular thermal shift assays, western blotting, and CUT&Tag profiling were used to identify molecular targets and define transcriptional reprogramming. Results 6′'-O-acSSD markedly suppressed cancer cell proliferation, migration, and invasion and elicited a transcriptional program distinct from that induced by SSD. Transcriptomic and biochemical analyses revealed preferential activation of ferroptosis-associated signatures, including enhanced lipid peroxidation. Mechanistically, 6′'-O-acSSD engaged STAT3, inhibited its phosphorylation, and extensively remodeled STAT3 chromatin occupancy. Functional analyses showed that STAT3 inhibition was required for the full anti-tumor activity of 6′'-O-acSSD. Notably, blockade of ferroptosis only partially rescued cell viability, whereas STAT3 targeting additionally triggered apoptosis-associated transcriptional and biochemical changes. The anti-tumor effects of 6′'-O-acSSD were further validated in patient-derived tumor organoids. Conclusion 6′'-O-acSSD exerts potent anti-tumor effects by targeting STAT3-dependent transcriptional programs and inducing coordinated ferroptosis and apoptosis. These findings highlight the therapeutic potential of structurally optimized natural products for anti-cancer treatment.
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JOURNAL OF ETHNOPHARMACOLOGY
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2025
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IF 5.4
Xiao Zhang,Zhekai Huang,Xuejun Hu,Yu Tang,Xiaofeng Zhong,Li Li,Liujing Ni,Fang Li,Haibing Hua,Fangshi Zhu
Ethnopharmacological relevance Wendan Decoction (WDD) is a classical prescription deeply rooted in traditional Chinese medicine (TCM), originally documented by Sun Simiao in Beiji Qianjin Yaofang during the Tang Dynasty. Traditionally, it has been used to treat disorders associated with phlegm-dampness accumulation and digestive dysfunction, reflecting the TCM principle of harmonizing the stomach and resolving dampness. Within the clinical practice at Jiangyin Hospital Affiliated to Nanjing University of Chinese Medicine, WDD is employed for the treatment of chronic atrophic gastritis (CAG), continuing its long-standing application in gastrointestinal disorders. Despite its widespread traditional use and cultural significance, the active constituents and precise pharmacological mechanisms of WDD have not yet been fully elucidated. Purpose This study aimed to systematically investigate the material basis and therapeutic mechanisms of WDD in CAG treatment. Methods The bioactive constituents of WDD were first identified using high-performance liquid chromatography coupled with quadrupole time-of-flight tandem mass spectrometry (HPLC-Q-TOF-MS/MS). To evaluate its therapeutic effects, we established both in vivo and in vitro models of chronic atrophic gastritis (CAG). For the in vivo studies, a rat CAG model was generated through a multi-factor compound induction approach, whereas in vitro cellular injury was induced using N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). To elucidate the underlying mechanisms, we integrated network pharmacology to predict candidate targets and signaling pathways, followed by experimental verification via immunohistochemical staining and Western blot analysis. Results HPLC-Q-TOF-MS/MS profiling revealed 34 bioactive constituents in WDD, with naringin, neohesperidin, and narirutin identified as key components. In vivo investigations demonstrated that WDD administration markedly improved gastric histopathological alterations in CAG model rats, accompanied by increased serum levels of pepsinogen I (PG I) and pepsinogen II (PG II), along with reduced gastrin-17 (G-17) and interleukin-6 (IL-6) concentrations. In vitro studies further showed that WDD treatment inhibited cell proliferation, migration, and invasive potential in MNNG-transformed MC cells. Network pharmacology-based analysis predicted that the therapeutic efficacy of WDD against CAG was primarily mediated via the JAK/STAT signaling axis. Subsequent mechanistic validation confirmed that WDD significantly attenuated the phosphorylation of JAK2 and STAT3, suggesting its inhibitory effect on the JAK2/STAT3 pathway. Conclusion This study revealed that WDD exerted therapeutic effects on CAG through suppression of the JAK2/STAT3 pathway. Our findings elucidate the pharmacological mechanisms of WDD and provide a scientific basis for its traditional use in managing CAG, highlighting its potential as a therapeutic candidate worthy of further clinical investigation.
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Frontiers in Pharmacology
·
2025
·
IF 4.8
Shuzhen Mao,Jiahui Huang,Junyan Li,Fang Sun,Qilian Zhang,Qing Cheng,Wei Zeng,Dongya Lei,Shiyan Wang,Jing Yao
Introduction: Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) characterized by mucosal damage and impaired epithelial barrier function. While glycyl-l-histidyl-l-lysine-copper (GHK-Cu) exhibits known anti-inflammatory properties, its therapeutic mechanisms in UC remain undefined. This study was designed to systematically evaluate the therapeutic potential of GHK-Cu in a dextran sulfate sodium (DSS)-induced murine model of UC, with particular emphasis on elucidating its regulatory effects on the NAD-dependent deacetylase sirtuin-1 (SIRT1)/signal transducer and activator of transcription 3 (STAT3) signaling pathway.Methods: UC was induced in BALB/c mice with 3% DSS for 14 days. The protein expression levels of tight junction associated protein-1 (ZO-1), Occludin, inflammatory factors interleukin (IL)-6, IL-1β and tumor necrosis factor (TNF)-α, SIRT1, STAT3, p-STAT3, and retinoic acid receptor-related orphan receptor gamma t (RORγt) were detected by Western blot. Histopathological changes were evaluated by Hematoxylin and Eosin (H&E) and Alcian blue-periodic acid-Schiff (AB-PAS). Network pharmacology and molecular docking were used to predict the core targets of GHK Cu in the treatment of UC. An in vitro UC model was also established in mouse peritoneal macrophages (MPMs) using lipopolysaccharide (LPS), and a co culture model was constructed using mouse colonic epithelial cells (MCECs) and MPMs to examine the role of GHK Cu in promoting mucosal healing. STAT3 was silenced by gene transfection technology to verify the core role of STAT3 in GHK Cu treatment of UC.Results: GHK-Cu alleviated weight loss, improved the disease activity index (DAI), reduced colonic edema and shortening, attenuated inflammatory damage, increased goblet cell numbers, suppressed inflammatory cytokines such as TNF-α, IL-6, and IL-1β, and promoted mucosal repair. Additionally, a co-culture system of MCECs and MPMs revealed that GHK-Cu facilitated MCECs healing, impaired by DSS, by upregulating ZO-1 and Occludin expression. Subsequently, network pharmacology and molecular docking identified SIRT1 as a potential target of GHK-Cu. Results showed that GHK-Cu upregulated SIRT1 protein expression and suppressed the expression of phosphorylated p-STAT3 in colon tissue and MCECs of the co-culture model. Our findings revealed that after transfection with STAT3-targeting siRNA (siSTAT3), the stimulant effect of GHK-Cu on the healing of MCECs and the effect on the protein expression of ZO-1 and Occludin is canceled. Nevertheless, after transfection with siSTAT3, it could inhibit the expression of inflammatory factors in conjunction with GHK-Cu. Furthermore, we found that GHK-Cu could inhibit RORγt expression in the colon tissue of UC mice.Discussion: This study found that GHK-Cu demonstrated significant therapeutic effects in DSS-induced UC in mice. GHK-Cu may promote mucosal healing and enhance tight junction protein expression by regulating the SIRT1/STAT3 pathway. In addition to suppressing p-STAT3 expression, GHK-Cu may utilize additional pathways to inhibit inflammatory factors. Furthermore, GHK-Cu may reduce the number of Th17 cells. In summary, GHK-Cu may treat UC by acting on the SIRT1/STAT3 pathway.
研究领域:
药理学
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免疫学
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分子生物学
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胃肠病学
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高影响因子
JOURNAL OF BIOMEDICAL SCIENCE
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2023
·Vol. 30
·期 1
·1-14
·
IF 11
Shen Weiyi,Shao Wentao,Wang Qihan,Wang Bo,Zhao Gang,Gu Aihua,Jiang Zhaoyan,Hu Hai
Background Cholesterol gallstone disease is a common disease. Reducing cholesterol burden is important to prevent/treat gallstone. In this study, we investigated the application of diosgenin (DG) to prevent the formation of gallstone in mice.Methods Adult male C57BL/6J mice were fed with the lithogenic diet (LD) only or LD supplemented with DG or ezetimibe for 8 weeks. Incidences of gallstone formation were documented. Intestine and liver tissues were collected to measure the lipid contents and expression of genes in cholesterol metabolism. Caco2 cells were treated with DG to monitor the regulation on cholesterol absorption and the transcriptional regulation of Npc1l1 gene. Changes of gut microbiota by DG was analyzed. Intraperitoneal injection of LPS on mice was performed to verify its effects on STAT3 activation and Npc1l1 expression in the small intestine.Results LD led to 100% formation of gallstones in mice. In comparison, dietary DG or ezetimibe supplementary completely prevents gallstones formation. DG inhibited intestinal cholesterol absorption in mice as well as in Caco2 cells by down-regulation of Npc1l1 expression. DG could directly inhibit phosphorylation of STAT3 and its transcriptional regulation of Npc1l1 expression. Furthermore, DG could modulate gut microbiota profiles and LPS mediated STAT3 activation and Npc1l1 expression.Conclusion Our results demonstrated that dietary DG could inhibit intestinal cholesterol absorption through decreasing NPC1L1 expression to prevent cholesterol gallstone formation.
研究领域:
药理学
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胃肠病学
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分子生物学
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高影响因子
Journal of Advanced Research
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2022
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IF 12.822
Ying Zhu,Anni Wang,Shuya Zhang,Jisu Kim,Jiaxuan Xia,Fengxue Zhang,Dan Wang,Qi Wang,Jianxin Wang
Introduction Inherent or acquired resistance to paclitaxel (PTX) is a pivotal challenge for chemotherapy treatment of multidrug-resistant (MDR) breast cancer. Although various targeted drug-delivery systems, including nanoparticles and liposomes, are effective for MDR cancer treatment, their efficacy is restricted by immunosuppressive tumor microenvironment (TME). Methods Ginsenosides Rg3 was used to formulate unique Rg3-based liposomes loaded with PTX to establish Rg3-PTX-LPs, which were prepared by the thin-film hydration method. The stability of the Rg3-PTX-LPs was evaluated by particle size analysis through dynamic light scattering. The active targeting effect of Rg3-based liposomes was examined in an MCF-7/T xenograft model by an in a vivo imaging system. To evaluate the antitumor activity and mechanism of Rg3-PTX-LP, MTT, apoptosis assays, TAM regulation, and TME remodeling were performed in MCF-7/T cells in vitro and in vivo. Results Rg3-PTX-LPs could specifically distribute to MCF7/T cancer cells and TME simultaneously, mainly through the recognition of GLUT-1. The drug resistance reversing capability and in vivo antitumor effect of Rg3-PTX-LPs were significantly improved compared with conventional cholesterol liposomes. The TME remodeling mechanisms of Rg3-PTX-LPs included inhibiting IL-6/STAT3/p-STAT3 pathway activation to repolarize protumor M2 macrophages to antitumor M1 phenotype, suppressing myeloid-derived suppressor cells (MDSCs), decreasing tumor-associated fibroblasts (TAFs) and collagen fibers in TME, and promoting apoptosis of tumor cells. Hence, through the dual effects of targeting tumor cells and TME remodeling, Rg3-PTX-LPs achieved a high tumor inhibition rate of 90.3%. Conclusion Our multifunctional Rg3-based liposome developed in the present study offered a promising strategy for rescuing the drug resistance tumor treatment.
研究领域:
药学
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肿瘤学
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纳米技术
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癌症治疗
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高影响因子
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
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2021
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IF 4.013
Yuanyuan Wu,Mengnan Zeng,Ruiqi Xu,Beibei Zhang,Shengchao Wang,Benke Li,Yuxuan Kan,Bing Cao,Xiaoke Zheng,Weisheng Feng
Background Melanoma is an aggressive cancer with a rapidly increasing incidence rate worldwide. Acteoside has been shown to have antitumor effects in multiple human cancers; however, the underlying function and mechanisms of acteoside in melanoma remain unclear. Purpose This study explored the inhibitory effect of acteoside on melanoma and the possible mechanisms. Methods Acteoside (15 mg/kg, 30 mg/kg) was administered to mice daily for 21 days. ICI182,780 (0.5 mg/kg) was intraperitoneally injected 30 min before acteoside administration three times a week to evaluate whether the effects elicited by acteoside were mediated via the estrogen receptor . Tumor growth and metabolism, cardiac function, ROS and apoptosis levels in the spleen, serum inflammatory factors, and immune cells in the spleen were monitored. STAT3 , p-STAT3, CD31 , and survivin levels in tumor tissues were measured via immunofluorescence. Ras, Raf1, STAT3, p-STAT3, Bcl-2, Bax, cleaved caspase-3, and cleaved caspase-9 levels in tumor tissues were determined via Western Blotting . Results The results showed that acteoside inhibited melanoma growth, alleviated inflammation levels in mice, attenuated ROS and apoptosis levels in the spleen, downregulated the levels of CD31, survivin, Ras, Raf1, p-STAT3, and Bcl-2, and upregulated the levels of ER β , Bax, cleaved caspase-3, and cleaved caspase-9. Moreover, the effect of acteoside was blocked by ICI182,780. Conclusion Acteoside may promote the apoptosis of tumor cells by regulating the ER β -Ras/Raf1-STAT3 signaling axis, thus inhibiting the occurrence and development of melanoma.
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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免疫学
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高影响因子
MOLECULAR CARCINOGENESIS
·
2018
·Vol. 58
·期 4
·565-576
·
IF 3.851
Hailun Zheng,Lehe Yang,Yanting Kang,Min Chen,Shichong Lin,Youqun Xiang,Caleb Li,Xuanxuan Dai,Xiaoying Huang,Guang Liang,Chengguang Zhao
Several studies have implicated the feedback activation of signal transducer and activator of transcription 3 (STAT3) as a new cancer drug-resistance mechanism and linked it to the failure of epidermal growth factor receptor (EGFR)-targeted therapies. In this study, we discovered that Alantolactone, a natural sesquiterpene lactone, potently inhibited human pancreatic cancer cells and suppressed constitutively activated STAT3. In contrast, Alantolactone had little effect on the EGFR pathway. Moreover, combination of Alantolactone and an EGFR inhibitor, Erlotinib or Afatinib, demonstrated a remarkable synergistic anti-cancer effect against pancreatic cancer cells both in vitro and in vivo. Our results suggested that Alantolactone could sensitize human pancreatic cancer cells to EGFR inhibitors possibly through down-regulating the STAT3 signaling. Alantolactone, when combined with other EGFR targeted agents, could be further developed as a potential therapy for pancreatic cancer.
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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DOI
PubMed
高影响因子
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