共查询到20条相似文献,搜索用时 46 毫秒
1.
《European journal of cancer (Oxford, England : 1990)》2014,50(17):2905-2915
AimAdjuvant chemotherapy has changed dramatically in the last decades. Anthracycline-/Taxane-based and dose-dense chemotherapy regimens improved survival in node positive breast cancer. This study tries to answer the following questions:
- (1)Are there differences in survival dependent on chemotherapy regimens in stratified by number of positive lymph nodes/grading (G)/hormone receptor-status (HR)/T-stage?
- (2)Is it possible to attribute these effects to chemotherapy by only investigating patients who received 100% guideline-conform surgery, radiotherapy and endocrine therapy?
2.
Jie Shen Lijun Xu Taofeek K. Owonikoko Shi-Yong Sun Fadlo R. Khuri Walter J. Curran Xingming Deng 《Cancer letters》2012
Cigarette smoking, either active or passive, is the most important risk factor in the development of human lung cancer. Mounting evidence indicates that cigarette smoke constituents not only contribute to tumorigenesis but also may increase the spread of cancer in the body. Nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is formed by nitrosation of nicotine and has been identified as the most potent carcinogen. NNK, an important component in cigarette smoke, may also promote tumor metastasis by regulating cell motility. Here we found that NNK can induce activation of a functionally interdependent protein kinase cascade, including c-Src, PKCι and FAK, in association with increased migration and invasion of human lung cancer cells. c-Src, PKCι and FAK are extensively co-localized in the cytoplasm. Treatment of cells with α7 nAChR specific inhibitor α-bungarotoxin (α-BTX) blocks NNK-stimulated activation of c-Src, PKCι and FAK and suppresses cell migration and invasion. Intriguingly, NNK enhances c-Src/PKCι and PKCι/FAK bindings, indicating a potential mechanism by which these kinases activate each other. Specific disruption of c-Src, PKCι or FAK expression by RNA interference significantly reduces NNK-induced cell migration and invasion. These findings suggest that NNK-induced migration and invasion may occur in a mechanism through activation of a c-Src/PKCι/FAK loop, which can contribute to metastasis and/or development of human lung cancer. 相似文献
3.
4.
5.
Suk-Bin Seo Jung-Gu Hur Mi-Ju Kim Jae-Won Lee Hak-Bong Kim Jae-Ho Bae Dong-Wan Kim Chi-Dug Kang Sun-Hee Kim 《Molecular cancer》2010,9(1):199
Background
The development of new modulator possessing high efficacy, low toxicity and high selectivity is a pivotal approach to overcome P-glycoprotein (P-gp) mediated multidrug resistance (MDR) in cancer treatment. In this study, we suggest a new molecular mechanism that TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) down-regulates P-glycoprotein (P-gp) through inhibition of DNA-PKcs/Akt/GSK-3β pathway and activation of caspases and thereby sensitize MDR cells to MDR-related drugs. 相似文献6.
Donglin Guo Hong Zhou Ying Wu Fang Zhou Guoying Xu Haiping Wen Xianmei Zhang 《Tumour biology》2011,32(5):921-930
Our previous study has demonstrated that TF/FVIIa and protease-activated receptor 2 (PAR2) are closely related to the proliferation
and migration of colon cancer cell line SW620. However, the detailed signaling cascades and underlying molecular mechanisms
remain unclear. This study has investigated whether extracellular signal-regulated kinase 1 and 2 (ERK1/2) and nuclear factor
kappaB (NF-κB) signaling pathways are involved in the events. The results revealed that PAR2-activating peptide (PAR2-AP)
or FVIIa elicited time-dependent upregulation of ERK1/2 phosphorylation in SW620 cells, and the effect of FVIIa was significantly
attenuated by anti-TF antibody. PAR2-AP or FVIIa also increased NF-κB (p65/RelA) levels among cell nuclear proteins and simultaneously
decreased IκB-α levels in the cytoplasmic proteins. Such effects of FVIIa can be inhibited with anti-PAR2 or anti-TF antibodies.
While ERK1/2 inhibitor (U0126) intervened with the regulatory effects of PAR2-AP and FVIIa on IκB-α/NF-κB (p65/Rel) expression
in the cells, NF-κB inhibitor (PDTC) partially blocked the enhancing effects of PAR2-AP and FVIIa on the proliferating and
migratory ability of SW620 cells. Furthermore, the regulatory effects of PAR2-AP and FVIIa on expressions of certain proteins
(IL-8, caspase-7, and TF) were also significantly abolished by PDTC. Collectively, the data in this study suggest that the
interaction between FVIIa and TF induces PAR2 activation, thereby triggers the ERK1/2 and IκB-α/NF-κB signal transduction
pathway to regulate the gene expression of IL-8, TF, and caspase-7, and ultimately promotes SW620 cell proliferation and migration. 相似文献
7.
Participation of Bcl-2/Bax-α in Glutamate-induced Apoptosis of Human Glioblastoma Cells 总被引:4,自引:0,他引:4
Nishi T Takahashi M Ito H Yoshihama I Takada E Mizuguchi J 《Journal of neuro-oncology》1999,44(2):109-117
Glutamate has been shown to function as a toxic agent in neuronal and glial cells, as well as an excitatory neurotransmitter throughout the central nervous system. In the present study, we examined the effect of increasing glutamate concentration on the induction of apoptosis in the two human glioblastoma cell lines GB-4 and GB-12. Glutamate exposure caused cell death of GB-4 and GB-12 in a dose-dependent manner. The cells were found to die via apoptosis in response to glutamate based on the following criteria: propidium iodide (PI) staining, H–E staining, electron microscopic analysis, and the TdT-mediated dUTP-biotin nick end labeling (TUNEL) method. The glutamate-induced apoptosis appears to involve the modulation of Bcl-2 family gene products such as Bcl-2, Bcl-xL, and Bax-. Both Bcl-2 and Bcl-xL were down-regulated by glutamate at 24 h and further at 48 h. The apoptosis-promoting product p21 Bax- was also down-regulated in GB-12 but slightly up-regulated in GB-4, accompanied by generation of variant form of p18 Bax- in both cell lines. These findings suggest that glutamate toxicity results in cellular death via an apoptotic mechanism which appears to involve the Bcl-2/Bax- molecular complex. 相似文献
8.
Astrid A.C. De Leeuw Jeroen B. Van de KamerMarinus A. Moerland Marielle E.P. PhilippensIna-M. Jürgenliemk-Schulz 《Radiotherapy and oncology》2011,101(2):337-342
Purpose
To evaluate the effect of different α/β and half-time of repair T½ on the assessment of clinical treatment plans for patients with cervical cancer.Materials and methods
We used EBRT and BT treatment plans of five patients, planned with MRI guided BT. We computed 3D EQD2 dose distributions of combined EBRT and BT treatments and calculated D90 of high-risk clinical target volume (HR-CTV) and D2cc for bladder and rectum, and the ratio D2cc(bladder)/D90(HR-CTV). BT was modelled as PDR (two applications of 32 × 60 cGy) and HDR (two applications of 2 × 7 Gy). We assumed a low, standard and high value for the biological parameters: HR-CTV α/β = 5/10/15 Gy and T½ = 0.5/1.5/2.5 h; OAR α/β = 2/3/4 Gy; T½ = 0.5/1.5/4.5 h.Results
The chosen variation in modelling parameters had a much larger effect on PDR treatments than on HDR treatments, especially for OAR, thus creating larger uncertainties. The relative mean range of the ratio D2cc(bladder)/D90(HR-CTV) is 72% for PDR and 25% for HDR. Out of the 125 modelled combinations 48 PDR plans and 23 HDR plans comply with clinical objectives.Conclusion
For HDR brachytherapy, only α/β has a significant impact on reported EQD2 values, whereas for PDR both α/β and T1/2 are important.Generally, the ratio D2cc(bladder)/D90(HR-CTV) is more favourable for PDR, even considering the larger uncertainties in EQD2. 相似文献9.
Changbao Chen Meng Zhao Aixian Tian Xiaolin Zhang Zhi Yao Xinlong Ma 《Oncotarget》2015,6(19):17570-17583
Bone sarcomas such as osteosarcoma and chondrosarcoma are frequently refractory to conventional chemotherapy and radiotherapy that exhibit poor prognosis. The Wnt signaling are evolutionarily conserved and implicated in cell proliferation and sarcomagenesis. However, the potential role of the Wnt signaling in bone sarcomas is still unclear. Here we demonstrate aberrant activation of Wnt/β-catenin signaling in bone sarcoma cells, involving an autocrine Wnt signaling loop with upregulation of specific Wnt ligands and receptors. Activation of Wnt/β-catenin signaling with Wnt3a or GSK-3β inhibitor drives the proliferation of bone sarcoma cells, whereas downregulation of activated Wnt signaling with dnTCF4 or siLEF1 suppresses bone sarcoma proliferation and induces cell cycle arrest. Taken together, our findings establish the evidence that aberrant activation of Wnt/β-catenin pathway involving an autocrine Wnt singaling drives the proliferation of bone sarcoma cells, and identify the autocrine activation of the Wnt/β-catenin signaling as a potential novel therapeutic target for bone sarcomas. 相似文献
10.
Objective To evaluate the 8th edition of AJCC/UICC staging system for stage Ⅲ nasopharyngeal carcinoma (NPC) by the survival analysis. All patients were treated with intensity-modulated radiotherapy (IMRT). Methods Among 1351 treatment-naïve NPC patients who received radiotherapy/chemoradiotherapy in our hospital from December 2008 to October 2014, 742 and 784 cases were classified as clinical stage Ⅲ based on the criteria of the 7th and 8th edition of AJCC/UICC staging systems, respectively. These patients were classified into three subgroups according to the 7th and 8th edition of AJCC/UICC staging systems:T3N0-1 as G1(n=226, n=245), T1-2N2 as G2(n=180, n=187) and T3N2 as G3(n=336, n=352). The 5-year overall survival (OS), progression-free survival (PFS), distant metastasis-free survival (DMFS) and local-regional recurrence-free survival (LRRFS) were analyzed with Kaplan-Meier method. The differences among different groups were evaluated by log-rank test. Results There were 93.6% patients evaluated by the 8th AJCC/UICC staging system remained the same cohort with those by the 7th AJCC/UICC staging system. The 5-year OS, PFS, DMFS and LRRFS of the 8th and 7th staging systems were 84.8% and 85.4%, 76.2% and 77.0%, 80.4% and 81.3%, 89.8% and 90.6%, respectively (all P>0.05). The OS, PFS or DMFS significantly differed among three subgroups classified by the 8th staging system (all P<0.001). In addition, statistical significance was observed between G1 and G2, and between G1 and G3(both P<0.05), whereas no statistical significance was noted between G2 and G3(P=0.183, 0.310, 0.248). Conclusions The distribution features and clinical endpoints of clinical stage Ⅲ defined by the 8th AJCC/UICC staging system are similar to those defined by the 7th AJCC/UICC staging system. The distribution of survival risk significantly differs among different subgroups. N2 plays a major role in assessing the survival risk of patients with stage Ⅲ NPC. In the era of IMRT plus chemotherapy, the effect of local tumors on clinical prognosis has been diminished. The 8th AJCC/UICC staging system remains to be further improved. 相似文献
11.
Mutations in oncogenes and tumor suppressor genes confer a fitness advantage to cells that can lead to cancer. The tumor phenotype normally results from the interaction of many mutant genes making it difficult to estimate the fitness advantage provided by any oncogene, except when tumors depend on one oncogene only. We utilize a model of chronic myeloid leukemia (CML), to quantitate the fitness advantage conferred by expression of BCR–ABL in hematopoietic cells from in vivo patient data. We show that BCR–ABL expression provides a high fitness advantage, which explains why this single mutation drives the chronic phase of CML. 相似文献
12.
13.
Ciarlo M Benelli R Barbieri O Minghelli S Barboro P Balbi C Ferrari N 《International journal of cancer. Journal international du cancer》2012,131(3):582-590
Current diagnostic tools cannot predict clinical failure and androgen‐independent disease progression for patients with prostate cancer (PC). The survival signaling pathways of prostate cells play a central role in the progression of tumors to a neuroendocrine (NE) phenotype. NE cells demonstrate attributes that suggest that they are an integral part of the signaling cascade leading to castration‐resistant PC. In this study, making use of in vitro neuroendocrine differentiation (NED) of human LNCaP and mouse TRAMP‐C2 cells after androgen withdrawal, and of the transgenic adenocarcinoma of mouse prostate (TRAMP) model, we characterized a sequence of molecular events leading to NED and identified a number of markers that could be detectable by routine analyses not only in castration resistant PC but also in hormone naïve PC at the time of initial diagnosis. We found that NED associates with AKT activation that in turn regulates heterogeneous nuclear ribonucleoprotein K (hnRNP K), androgen receptor (AR) and β‐catenin levels. Addition of molecules targeting membrane‐bound receptors and protein kinases blocks NE differentiation in LNCaP and TRAMP‐C2 cells. The extent of AKT phosphorylation and hnRNP K, AR and β‐catenin levels may have a potential value as prognostic indicators discriminating between androgen‐responsive and unresponsive cells and could be used as molecular targets to monitor the anti‐tumor action of new therapeutic protocols based on antireceptor agents and/or neuroendocrine hormone antagonists. 相似文献
14.
Sanket Mehta Lilian Schwarz John Spiliotis Mao-Chih Hsieh Eduardo H. Akaishi Diane Goere Paul H. Sugarbaker Dario Baratti François Quenet David L. Bartlett Laurent Villeneuve Vahan Kepenekian 《European journal of surgical oncology》2018,44(11):1786-1792
Introduction
Peritoneal metastasis (PM) of hepatocellular carcinoma (HCC) without distant spread are rare. The related prognosis is poor without standard treatment available. The role of cytoreduction surgery (CRS) and hyperthermic intraperitoneal chemotherapy (HIPEC) is poorly documented.Methods
An international multicentric cohort was constituted by retrospective analysis of 21 patients undergoing CRS/HIPEC for PM of HCC between 1992 and 2016 from 10 reference centers of PSOGI. Data on clinical features, treatment strategies, and survival outcomes were analyzed.Results
The median time interval from the diagnosis of PM to the procedure was 4.5 months. The median peritoneal cancer index was 14. Sixteen patients had complete cytoreduction (CCR0-1). Ten patients had grades 3 to 4 complications. The median duration of follow-up was 52.2 months. The median OS was 46.7 months. The projected 3y-OS and 5y-OS were 88.9 and 49.4% respectively. The median OS for patients with CCR0-1 resection was not reached whereas it was 5.9 months for those with CCR2-3 resection after CRS (p = 0.0005). The median RFS was 26.3 months and projected RFS at 3 years of 36.5 months Three prognostic factors were associated with improved RFS in the univariate analysis: preoperative chemotherapy (p = 0.0156), PCI >15 (p = 0.009), Number of chemotherapy agents used for HIPEC (p = 0.005).Conclusion
CRS/HIPEC is a safe and effective approach in selected patients with PM of HCC. CRS/HIPEC gives the patient a chance for a good relapse free and overall survival and should be considered as an option. 相似文献15.
Objective: To explore the expression and meaning of Toll-like receptor 2/4 in alveolar macrophage during the process of total hepatic ischemia in mice. Methods: BALB/c mice were used in a model of total hepatic ischemia/reperfusion. Alveolar Macrophage were collected at the time point of lh, 6h and 12h by the means of bronchoalveolar lavage (BAL), and its TLR2/4 mRNA and protein were detected with Flow Cytometry and Real-time PCR. The level of TNF in BAL fluid were measured. The concentration of MPO, the ratio of wet/dry and lung histological scores were used to assess the degrees of lung injuries. Results: At the three time points of hepatic ischemia reperfusion, the expression of TLR2/4 protein of and mRNA were up-regulated and the level of TLR2 was on the rise continually. TLR4 at the time of 6 h reached the peak value (P〈0.01). The level of TNF-2 in BAL fluid reached the highest point at the time of 6 h (P〈0.01). The ratio of wet/dry rose continually during hepatic ischemia reperfusion. After 1 h, the level of MPO increased rapidly. Then it reached the peak value during the period of 6 h to 12 h. Conclusion: TLR2/4 on the mice of alveolar macrophage were activated in the process of hepatic ischemia/reperfusion and involved in the injury of lung. 相似文献
16.
Hoeller U Tribius S Kuhlmey A Grader K Fehlauer F Alberti W 《International journal of radiation oncology, biology, physics》2003,55(4):1013-1018
PURPOSE: The Radiation Therapy Oncology Group (RTOG) and Late Effects Normal Tissue Task Force subjective, objective, management, and analytic (LENT/SOMA) scores were compared in a group of breast cancer patients. The impact of the classification system on grading late effects was evaluated. MATERIALS AND METHODS: Telangiectasia, skin pigmentation, and fibrosis were scored according to both LENT/SOMA and RTOG criteria. The results were compared with respect to up- or downgrading and correlated (Spearman's rho). Other side effects were recorded using LENT/SOMA criteria. Interobserver variability was calculated with Cohen's kappa. Two hundred fifty-nine subsequent relapse-free patients who underwent breast-conserving therapy between 1981 and 1995 were examined. The median dose of radiotherapy to the breast was 55 Gy. Adjuvant chemotherapy was given to 31 patients and tamoxifen to 52 patients. The median follow-up was 8 years. RTOG skin and s.c. tissue scales and LENT/SOMA breast and pigmentation scales were used. Two doctors examined 45 patients jointly. RESULTS: Of all patients, 20% had telangiectasia, 22% pigmentation, 43% fibrosis, 4% breast edema, 77% retraction/atrophy, and 54% pain. In comparison, when LENT/SOMA criteria were used, telangiectasia and pigmentation were upgraded in 34% and 36%, respectively, and telangiectasia was downgraded in 45%. Fibrosis correlated well (Spearman's rho 0.78, p = 0.01). An additional 356 side effects, mainly retraction/atrophy were observed in 226 patients using LENT/SOMA criteria. Interobserver variability was similar for both classification systems and ranged from Cohen's kappa 0.3 (retraction) to 0.91 (telangiectasia). CONCLUSIONS: LENT/SOMA criteria seem to be the better tool in grading and recording late radiation toxicity compared with the RTOG scale. There was some upgrading with the RTOG score when skin toxicity is evaluated. In contrast, fibrosis scores correlated very well. Adjustments of the LENT/SOMA scoring system should be considered to standardize reporting of late radiation morbidity. 相似文献
17.
Wang Lixue Wang Haojie Ouyang Weiwei Yang Wengang Ma Zhu Li Qingsong Li Huiqin Chen Xiaxia Li Xiaoyang Geng Yichao Su Shengfa Lu Bing 《中华放射肿瘤学杂志》2010,29(9):751-756
Objective To explore the possibility of CD+4 T cells and CD+4/CD+8 ratio in peripheral blood to predict the survival of patients with stage Ⅳ non-small cell lung cancer (NSCLC), and to establish a Nomogram prediction model. Methods The influence of CD+4 T cells and CD+4/CD+8 ratio on the clinical factors and survival of 682 patients pathologically diagnosed with stage Ⅳ NSCLC with no history of cancer treatment was retrospectively analyzed and the Nomogram prediction model was established. Combined with the changes of immune cells levels in 110 patients after treatment, the prognostic and predictive values of CD+4 T cells and CD+4/CD+8 ratio were verified. Countable data were analyzed by t-test. The survival rate was calculated by Kaplan-Meier method, log-rank test or univariate analysis. The multivariate analysis was performed by Cox regression model. Results Univariate analysis demonstrated that CD+4> 43.15% before treatment significantly prolonged the survival. By multivariate analysis of Cox regression model, CD+4>43.15% was an independent prognostic factor to prolong survival for stage Ⅳ NSCLC. The Nomogram model was established and verified that the predicted and actual overall survivals were highly consistent. Further analysis showed that 43.15% as the critical value of CD+4T cell level significantly prolonged survival when CD+4 expressed at a high-level before treatment, after treatment, before and after treatment, or combined with CD+4/CD+8>1.65. Conclusions The baseline level of CD+4 T cells before treatment in peripheral blood is an independent prognostic factor for stage Ⅳ NSCLC. The CD+4/CD+8 ratio before treatment has limited value in predicting the prognosis. 相似文献
18.
Dongliang Yan Enping Hu Haitao Zhang Sheng Liu Hairong Cai Lei Zhang Yan Zhou 《中国肿瘤临床(英文版)》2007,4(5):347-350
OBJECTIVE To investigate the diagnostic value of modified prostate specific antigen(PSA)parameters in the diagnosis of prostate cancer(PCA) when the serum PSAis in a grey zone of 4~10 ng/ml. METHODS The results of serum PSA determinations of the patients receiving a transrectal ultrasound-guided multiphase prostatic biopsy,were retrospectively analyzed.In the 88 patients with a serum PSA value of 4-10 ng/ml,the final diagnosis of PCA was made in 21,and that of benign prostate hyperplasia(BPH)in 67 patients.The percentage of the free-serum PSA([FPSA]/total-serum PSA[TPSA],F/T),PSA density(PSAD)and the sensitivity and specificity of the new PSA modified parameter(F/T)/PSAD in diagnosing PCA,within a set threshold value,was compared. RESULTS In the 88 patients with serum PSA in the grey zone of 4.0-10.0 ng/ml,there was no significant difference in comparing the TPSA between the 21 PCA patients and 67 BPH patients(P>0.05).However, there was a significant difference in the value of modified PSA parameters, such as F/T,PSAD and(F/T)/PSAD,between the PCA and the BPH groups (P<0.001).As the cut off point-value of the F/T,PSAD and(F/T)/PSAD was set at 0.16,0.15 and 0.8,the diagnostic sensitivity for PCA was 66.7%, 76.2%and 85.7%,and the specificity was 41.8%,43.3%and 68.7%,respectively.There was no significant difference in the sensitivity comparing the modified parameters for diagnosing PCA(P>0.05),whereas an overt predominance was present in the specificity of(F/T)/PSAD for PCAdiagnosis (P<0.05). CONCLUSION In the serum PSA grey zone of 4-10 ng/ml,a modified PSA parameter can improve the PCA diagnostic accuracy rate.With a considerably high sensitivity,application of the(F/T)/PSAD may effectively enhance the diagnostic specificity,which is superior to the F/T and PSAD, and can be expected to be one of the new indices derived from the PSA. 相似文献
19.
20.
Yuan Gao Zan Liu Xiuwei Zhang Jiani He Yongqi Pan Fengxia Hao Lingling Xie Qingchang Li Xueshan Qiu Enhua Wang 《Cancer letters》2013
Cisplatin-based chemotherapy is recommended as the first-line therapy for advanced non-small cell lung cancer (NSCLC). However, acquired cisplatin resistance is ubiquitous in patients with NSCLC, but the molecular mechanism of such resistance remains ambiguous. The present study sought to examine the role of the Wnt/β-catenin signaling pathway in cisplatin resistance by assessing the phosphorylation and subcellular distribution of GSK-3β in a human lung adenocarcinoma cell line, A549, and its cisplatin-resistant subline, A549/DDP. Total GSK-3β, phosphorylated GSK-3βser9 and phosphorylated GSK-3βtyr216 in cytoplasmic and nuclear fractions of A549/DDP and A549 cells were examined by western blot analysis. The regulation of cisplatin resistance, apoptosis, β-catenin and survivin protein expression by inhibition of cytoplasmic GSK-3β were determined by MTT assay, flow cytometry analysis, immunofluorescence technique and western blot analysis. In the present study, cytoplasmic levels of p-GSK-3βser9 were significantly increased in A549/DDP cells as compared with A549 cells (P < 0.01), and these levels were further increased by cisplatin treatment in A549/DDP cells (P < 0.01). In contrast, cytoplasmic levels of p-GSK-3βser9 were reduced in A549 cells after treatment with cisplatin (P < 0.01). However, cytoplasmic levels of p-GSK-3βtyr216 were significantly decreased in A549/DDP cells as compared with A549 cells (P < 0.01), and these levels were further decreased by cisplatin treatment in A549/DDP cells (P < 0.01). Conversely, cytoplasmic levels of p-GSK-3βtyr216 were raised in A549 cells after treatment with cisplatin (P < 0.01). Analysis of downstream effectors of the Wnt/β-catenin signaling pathway revealed upregulation of β-catenin and survivin expression in A549/DDP cells treated with cisplatin as compared to untreated cells. In A549 cells, cisplatin treatment decreased the expression of β-catenin and survivin. Furthermore, phosphorylation of GSK-3β at serine 9 by LiCl and transient interference of GSK-3β by siRNA increased β-catenin and survivin protein expression in A549/DDP cells. Low exogenous and endogenous cytoplasmic GSK-3β expression enhanced the IC50 and inhibited apoptosis. In conclusion, activation of the Wnt/β-catenin signaling pathway and upregulated survivin expression due to cytoplasmic GSK-3β inhibition might lead to cisplatin resistance in NSCLC. 相似文献