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Pulmonary cryptococcosis in the non-human immunodeficiency virus-infected population is uncommon. We aimed to explore the relevance between clinical presentations, radiological findings, and comorbidities and identify the outcome predictors. A total of 321 patients at Taichung Veterans General Hospital between 2005 and 2019 were included; of them, 204 (63.6%) had at least one comorbidity, while 67 (20.9%) had two or more. The most common comorbidities were diabetes mellitus (27.4%), malignant solid tumor (19.6%), autoimmune disease (15.6%), and chronic kidney disease (8.4%). Patients experiencing comorbidity, particularly those with multiple comorbidities, had a higher multilobar and extrapulmonary involvement, which could explain these patients being more symptomatic. In the overall population, extrapulmonary involvement independently predicted disease recurrence and death. Amongst patients with isolated pulmonary cryptococcosis, age, cryptococcal antigen (CrAg) titer in blood, and comorbidities not only predicted the extent of disease, but also its outcome. Of note, patients simultaneously with age ≥ 65 years, CrAg test ≥ 1:128, and multiple comorbidities had the lowest disease control of antifungal treatment (76.9%) and the highest rate of disease recurrence or death from any cause (40.0%). In conclusion, approximately two-thirds of patients had at least one underlying comorbidity. In addition to extrapulmonary involvement, old age, high CrAg titer in blood, and multiple comorbidities could act as risk factors for predicting the extent of disease and outcome.
Chun Lin; Tsung-Ying Yang; Ming-Cheng Chan; Kuo-Hsuan Hsu; Yen-Hsiang Huang; Jeng-Sen Tseng. Comprehensive Analysis and Risk Identification of Pulmonary Cryptococcosis in Non-HIV Patients. Journal of Fungi 2021, 7, 657 .
AMA StyleChun Lin, Tsung-Ying Yang, Ming-Cheng Chan, Kuo-Hsuan Hsu, Yen-Hsiang Huang, Jeng-Sen Tseng. Comprehensive Analysis and Risk Identification of Pulmonary Cryptococcosis in Non-HIV Patients. Journal of Fungi. 2021; 7 (8):657.
Chicago/Turabian StyleChun Lin; Tsung-Ying Yang; Ming-Cheng Chan; Kuo-Hsuan Hsu; Yen-Hsiang Huang; Jeng-Sen Tseng. 2021. "Comprehensive Analysis and Risk Identification of Pulmonary Cryptococcosis in Non-HIV Patients." Journal of Fungi 7, no. 8: 657.
The impact of different first-line epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI)s to the clinical efficacy of osimertinib in EGFR-mutant non-small-cell lung cancer (NSCLC) patients with acquired T790M was still unclear. We enrolled 733 advanced EGFR-mutant NSCLC patients with gefitinib, erlotinib or afatinib as first-line EGFR-TKIs treatment for analysis. 373 patients received re-biopsies after progressive disease to first-line EGFR-TKIs treatment, and the total positive rate of T790M was 51.7%. 151 patients who harbored T790M received osimertinib as subsequent treatment. Among them, the median progression-free survival (PFS) of first-line EGFR-TKI (PFS1) was 14.0 months, and the median PFS of osimertinib (PFS2) was 10.1 months. The median PFS1 + PFS2 was 27.5 months, and the median overall survival from first-line EGFR-TKI was 61.3 months. Concerning different first-line EGFR-TKIs, the median PFS2 was 10.9 months in the gefitinib group, 10.0 months in the erlotinib group, and 6.7 months in the afatinib group (p = 0.534). The median PFS1 + PFS2 was 27.7 months, 26.8 months and 24.0 months in the gefitinib, erlotinib, and afatinib group, respectively (p = 0.575). In conclusion, both first-generation and second-generation EGFR-TKIs sequential osimertinib treatment provided good clinical efficacy in advanced EGFR-mutant NSCLC patients with acquired T790M mutation.
Yen-Hsiang Huang; Jeng-Sen Tseng; Kuo-Hsuan Hsu; Kun-Chieh Chen; Kang-Yi Su; Sung-Liang Yu; Jeremy J. W. Chen; Tsung-Ying Yang; Gee-Chen Chang. The impact of different first-line EGFR-TKIs on the clinical outcome of sequential osimertinib treatment in advanced NSCLC with secondary T790M. Scientific Reports 2021, 11, 1 -10.
AMA StyleYen-Hsiang Huang, Jeng-Sen Tseng, Kuo-Hsuan Hsu, Kun-Chieh Chen, Kang-Yi Su, Sung-Liang Yu, Jeremy J. W. Chen, Tsung-Ying Yang, Gee-Chen Chang. The impact of different first-line EGFR-TKIs on the clinical outcome of sequential osimertinib treatment in advanced NSCLC with secondary T790M. Scientific Reports. 2021; 11 (1):1-10.
Chicago/Turabian StyleYen-Hsiang Huang; Jeng-Sen Tseng; Kuo-Hsuan Hsu; Kun-Chieh Chen; Kang-Yi Su; Sung-Liang Yu; Jeremy J. W. Chen; Tsung-Ying Yang; Gee-Chen Chang. 2021. "The impact of different first-line EGFR-TKIs on the clinical outcome of sequential osimertinib treatment in advanced NSCLC with secondary T790M." Scientific Reports 11, no. 1: 1-10.
RAGE (receptor for advanced glycation end-product) is thought to be associated with metastasis and poor prognosis of various types of cancer. However, RAGE is constitutively expressed in the normal lung and down-regulated in cancerous lung, while the opposite evidence shows that RAGE-mediated signaling contributes to the tumorigenesis of lung cancer. Therefore, the role of RAGE in lung cancer progression is still unclear to be further investigated. In this study, RAGE-overexpressed stable clones of human lung cancer A549 cells and two local lung adenocarcinoma cell lines CL1-0 and CL1-5 were utilized to verify the effect of RAGE on lung cancer cells while the in vivo xenograft animal model was further performed to evaluate the role of RAGE in the progression of lung cancer. The growth of A549 cells was inhibited by RAGE overexpression. p53-dependent p21CIP1 expression contributed to RAGE-induced growth inhibition by suppressing CDK2 kinase activity and retinoblastoma protein (RB) phosphorylation in vitro. On the other hand, RAGE overexpression promoted migration, invasion, and mesenchymal features of lung adenocarcinoma cells through ERK signaling. Furthermore, an in vivo xenograft experiment indicated that RAGE promoted the metastasis of lung cancer cells with p21CIP1 up-regulation, ERK activation, and the changes of EMT markers. Regarding to the involvement of tumor-associated macrophage (TAM) in the microenvironment, we monitored the expressions of TAM markers including CD68 and CD163 as well as angiogenesis marker CD31 in xenograft slice. The data showed that RAGE might induce the accumulation of TAM in lung cancer cells and further accelerate the in vivo tumor growth. In summary, our study provides evidence indicating the distinct in vitro and in vivo effects of RAGE and related mechanisms on tumor growth and metastasis, which shed light on the oncogenic role of RAGE in lung cancer.
Mei-Chih Chen; Kun-Chieh Chen; Gee-Chen Chang; Ho Lin; Chun-Chi Wu; Wei-Hsiang Kao; Chieh-Lin Jerry Teng; Shih-Lan Hsu; Tsung-Ying Yang. RAGE acts as an oncogenic role and promotes the metastasis of human lung cancer. Cell Death & Disease 2020, 11, 1 -13.
AMA StyleMei-Chih Chen, Kun-Chieh Chen, Gee-Chen Chang, Ho Lin, Chun-Chi Wu, Wei-Hsiang Kao, Chieh-Lin Jerry Teng, Shih-Lan Hsu, Tsung-Ying Yang. RAGE acts as an oncogenic role and promotes the metastasis of human lung cancer. Cell Death & Disease. 2020; 11 (4):1-13.
Chicago/Turabian StyleMei-Chih Chen; Kun-Chieh Chen; Gee-Chen Chang; Ho Lin; Chun-Chi Wu; Wei-Hsiang Kao; Chieh-Lin Jerry Teng; Shih-Lan Hsu; Tsung-Ying Yang. 2020. "RAGE acts as an oncogenic role and promotes the metastasis of human lung cancer." Cell Death & Disease 11, no. 4: 1-13.
Risk factors including genetic effects are still being investigated in lung adenocarcinoma (LUAD). Mitochondria play an important role in controlling imperative cellular parameters, and anomalies in mitochondrial function might be crucial for cancer development. The mitochondrial genomic aberrations found in lung adenocarcinoma and their associations with cancer development and progression are not yet clearly characterized. Here, we identified a spectrum of mitochondrial genome mutations in early-stage lung adenocarcinoma and explored their association with prognosis and clinical outcomes. Next-generation sequencing was used to reveal the mitochondrial genomes of tumor and conditionally normal adjacent tissues from 61 Stage 1 LUADs. Mitochondrial somatic mutations and clinical outcomes including relapse-free survival (RFS) were analyzed. Patients with somatic mutations in the D-loop region had longer RFS (adjusted hazard ratio, adjHR = 0.18, p = 0.027), whereas somatic mutations in mitochondrial Complex IV and Complex V genes were associated with shorter RFS (adjHR = 3.69, p = 0.012, and adjHR = 6.63, p = 0.002, respectively). The risk scores derived from mitochondrial somatic mutations were predictive of RFS (adjHR = 9.10, 95%CI: 2.93–28.32, p < 0.001). Our findings demonstrated the vulnerability of the mitochondrial genome to mutations and the potential prediction ability of somatic mutations. This research may contribute to improving molecular guidance for patient treatment in precision medicine.
Lovely Raghav; Ya-Hsuan Chang; Yi-Chiung Hsu; Yu-Cheng Li; Chih-Yi Chen; Tsung-Ying Yang; Kun-Chieh Chen; Kuo-Hsuan Hsu; Jeng-Sen Tseng; Cheng-Yen Chuang; Mei-Hsuan Lee; Chih-Liang Wang; Huei-Wen Chen; Sung-Liang Yu; Sheng-Fang Su; Shin-Sheng Yuan; Jeremy J.W. Chen; Shinn-Ying Ho; Ker-Chau Li; Pan-Chyr Yang; Gee-Chen Chang; Hsuan-Yu Chen. Landscape of Mitochondria Genome and Clinical Outcomes in Stage 1 Lung Adenocarcinoma. Cancers 2020, 12, 755 .
AMA StyleLovely Raghav, Ya-Hsuan Chang, Yi-Chiung Hsu, Yu-Cheng Li, Chih-Yi Chen, Tsung-Ying Yang, Kun-Chieh Chen, Kuo-Hsuan Hsu, Jeng-Sen Tseng, Cheng-Yen Chuang, Mei-Hsuan Lee, Chih-Liang Wang, Huei-Wen Chen, Sung-Liang Yu, Sheng-Fang Su, Shin-Sheng Yuan, Jeremy J.W. Chen, Shinn-Ying Ho, Ker-Chau Li, Pan-Chyr Yang, Gee-Chen Chang, Hsuan-Yu Chen. Landscape of Mitochondria Genome and Clinical Outcomes in Stage 1 Lung Adenocarcinoma. Cancers. 2020; 12 (3):755.
Chicago/Turabian StyleLovely Raghav; Ya-Hsuan Chang; Yi-Chiung Hsu; Yu-Cheng Li; Chih-Yi Chen; Tsung-Ying Yang; Kun-Chieh Chen; Kuo-Hsuan Hsu; Jeng-Sen Tseng; Cheng-Yen Chuang; Mei-Hsuan Lee; Chih-Liang Wang; Huei-Wen Chen; Sung-Liang Yu; Sheng-Fang Su; Shin-Sheng Yuan; Jeremy J.W. Chen; Shinn-Ying Ho; Ker-Chau Li; Pan-Chyr Yang; Gee-Chen Chang; Hsuan-Yu Chen. 2020. "Landscape of Mitochondria Genome and Clinical Outcomes in Stage 1 Lung Adenocarcinoma." Cancers 12, no. 3: 755.
Cyclin-dependent kinase 5 (CDK5) is a unique member of the cyclin-dependent kinase family. CDK5 is activated by binding with its regulatory proteins, mainly p35, and its activation is essential in the development of the central nervous system (CNS) and neurodegeneration. Recently, it has been reported that CDK5 plays important roles in regulating various biological and pathological processes, including cancer progression. Concerning prostate cancer, the androgen receptor (AR) is majorly involved in tumorigenesis, while CDK5 can phosphorylate AR and promotes the proliferation of prostate cancer cells. Clinical evidence has also shown that the level of CDK5 is associated with the progression of prostate cancer. Interestingly, inhibition of CDK5 prevents prostate cancer cell growth, while drug-triggered CDK5 hyperactivation leads to apoptosis. The blocking of CDK5 activity by its small interfering RNAs (siRNA) or Roscovitine, a pan-CDK inhibitor, reduces the cellular AR protein level and triggers the death of prostate cancer cells. Thus, CDK5 plays a crucial role in the growth of prostate cancer cells, and AR regulation is one of the important pathways. In this review paper, we summarize the significant studies on CDK5-mediated regulation of prostate cancer cells. We propose that the CDK5–p35 complex might be an outstanding candidate as a diagnostic marker and potential target for prostate cancer treatment in the near future.
Muhammet Oner; Eugene Lin; Mei-Chih Chen; Fu-Ning Hsu; G. M. Shazzad Hossain Prince; Kun-Yuan Chiu; Chieh-Lin Jerry Teng; Tsung-Ying Yang; Hsin-Yi Wang; Chia-Herng Yue; Ching-Han Yu; Chih-Ho Lai; Jer-Tsong Hsieh; Ho Lin. Future Aspects of CDK5 in Prostate Cancer: From Pathogenesis to Therapeutic Implications. International Journal of Molecular Sciences 2019, 20, 3881 .
AMA StyleMuhammet Oner, Eugene Lin, Mei-Chih Chen, Fu-Ning Hsu, G. M. Shazzad Hossain Prince, Kun-Yuan Chiu, Chieh-Lin Jerry Teng, Tsung-Ying Yang, Hsin-Yi Wang, Chia-Herng Yue, Ching-Han Yu, Chih-Ho Lai, Jer-Tsong Hsieh, Ho Lin. Future Aspects of CDK5 in Prostate Cancer: From Pathogenesis to Therapeutic Implications. International Journal of Molecular Sciences. 2019; 20 (16):3881.
Chicago/Turabian StyleMuhammet Oner; Eugene Lin; Mei-Chih Chen; Fu-Ning Hsu; G. M. Shazzad Hossain Prince; Kun-Yuan Chiu; Chieh-Lin Jerry Teng; Tsung-Ying Yang; Hsin-Yi Wang; Chia-Herng Yue; Ching-Han Yu; Chih-Ho Lai; Jer-Tsong Hsieh; Ho Lin. 2019. "Future Aspects of CDK5 in Prostate Cancer: From Pathogenesis to Therapeutic Implications." International Journal of Molecular Sciences 20, no. 16: 3881.
Arecoline is the primary alkaloid in betel nuts, which are known as a risk factor for oral submucosal fibrosis and oral cancer. Lung cancer is a severe type of carcinoma with high cell motility that is difficult to treat. However, the detailed mechanisms of the correlation between Arecoline and lung cancer are not fully understood. Here, we investigated the effect of Arecoline on migration in lung cancer cell lines and its potential mechanism through the muscarinic acetylcholine receptor 3 (mAChR3)-triggered EGFR/Src/FAK pathway. Our results indicate that different concentrations of Arecoline treatment (10 µM, 20 µM, and 40 µM) significantly increased the cell migration ability in A549 and CL1-0 cells and promoted the formation of the filamentous actin (F-actin) cytoskeleton, which is a crucial element for cell migration. However, migration of H460, CL1-5, and H520 cell lines, which have a higher migration ability, was not affected by Arecoline treatment. The EGFR/c-Src/Fak pathway, which is responsible for cell migration, was activated by Arecoline treatment, and a decreased expression level of E-cadherin, which is an epithelial marker, was observed in Arecoline-treated cell lines. Blockade of the EGFR/c-Src/Fak pathway with the inhibitors of EGFR (Gefitinib) or c-Src (Dasatinib) significantly prevented Arecoline-promoted migration in A549 cells. Gefitinib or Dasatinib treatment significantly disrupted the Arecoline-induced localization of phospho-Y576-Fak during focal adhesion in A549 cells. Interestingly, Arecoline-promoted migration in A549 cells was blocked by a specific mAChR3 inhibitor (4-DAMP) or a neutralizing antibody of matrix metalloproteinase (MMP7 or Matrilysin). Taken together, our findings suggest that mAChR3 might play an essential role in Arecoline-promoted EGFR/c-Src/Fak activation and migration in an A549 lung cancer cell line.
Chih-Hsiang Chang; Mei-Chih Chen; Te-Huan Chiu; Yu-Hsuan Li; Wan-Chen Yu; Wan-Ling Liao; Muhammet Oner; Chang-Tze Ricky Yu; Chun-Chi Wu; Tsung-Ying Yang; Chieh-Lin Jerry Teng; Kun-Yuan Chiu; Kun-Chien Chen; Hsin-Yi Wang; Chia-Herng Yue; Chih-Ho Lai; Jer-Tsong Hsieh; Ho Lin. Arecoline Promotes Migration of A549 Lung Cancer Cells through Activating the EGFR/Src/FAK Pathway. Toxins 2019, 11, 185 .
AMA StyleChih-Hsiang Chang, Mei-Chih Chen, Te-Huan Chiu, Yu-Hsuan Li, Wan-Chen Yu, Wan-Ling Liao, Muhammet Oner, Chang-Tze Ricky Yu, Chun-Chi Wu, Tsung-Ying Yang, Chieh-Lin Jerry Teng, Kun-Yuan Chiu, Kun-Chien Chen, Hsin-Yi Wang, Chia-Herng Yue, Chih-Ho Lai, Jer-Tsong Hsieh, Ho Lin. Arecoline Promotes Migration of A549 Lung Cancer Cells through Activating the EGFR/Src/FAK Pathway. Toxins. 2019; 11 (4):185.
Chicago/Turabian StyleChih-Hsiang Chang; Mei-Chih Chen; Te-Huan Chiu; Yu-Hsuan Li; Wan-Chen Yu; Wan-Ling Liao; Muhammet Oner; Chang-Tze Ricky Yu; Chun-Chi Wu; Tsung-Ying Yang; Chieh-Lin Jerry Teng; Kun-Yuan Chiu; Kun-Chien Chen; Hsin-Yi Wang; Chia-Herng Yue; Chih-Ho Lai; Jer-Tsong Hsieh; Ho Lin. 2019. "Arecoline Promotes Migration of A549 Lung Cancer Cells through Activating the EGFR/Src/FAK Pathway." Toxins 11, no. 4: 185.
Treatment for advanced EGFR-mutant lung adenocarcinoma patients displaying a higher PD-L1 expression level experienced a higher frequency of primary resistance to EGFR-TKIs.
Kuo-Hsuan Hsu; Yen-Hsiang Huang; Jeng-Sen Tseng; Kun-Chieh Chen; Wen-Hui Ku; Kang-Yi Su; Jeremy J.W. Chen; Huei-Wen Chen; Sung-Liang Yu; Tsung-Ying Yang; Gee-Chen Chang. High PD-L1 expression correlates with primary resistance to EGFR-TKIs in treatment naïve advanced EGFR-mutant lung adenocarcinoma patients. Lung Cancer 2019, 127, 37 -43.
AMA StyleKuo-Hsuan Hsu, Yen-Hsiang Huang, Jeng-Sen Tseng, Kun-Chieh Chen, Wen-Hui Ku, Kang-Yi Su, Jeremy J.W. Chen, Huei-Wen Chen, Sung-Liang Yu, Tsung-Ying Yang, Gee-Chen Chang. High PD-L1 expression correlates with primary resistance to EGFR-TKIs in treatment naïve advanced EGFR-mutant lung adenocarcinoma patients. Lung Cancer. 2019; 127 ():37-43.
Chicago/Turabian StyleKuo-Hsuan Hsu; Yen-Hsiang Huang; Jeng-Sen Tseng; Kun-Chieh Chen; Wen-Hui Ku; Kang-Yi Su; Jeremy J.W. Chen; Huei-Wen Chen; Sung-Liang Yu; Tsung-Ying Yang; Gee-Chen Chang. 2019. "High PD-L1 expression correlates with primary resistance to EGFR-TKIs in treatment naïve advanced EGFR-mutant lung adenocarcinoma patients." Lung Cancer 127, no. : 37-43.
Retinoic acid which belongs to the retinoid class of chemical compounds is an important metabolite of vitamin A in diets. It is currently understood that retinoic acid plays important roles in cell development and differentiation as well as cancer treatment. Lung, prostate, breast, ovarian, bladder, oral, and skin cancers have been demonstrated to be suppressed by retinoic acid. Our results also show that low doses and high doses of retinoic acid may respectively cause cell cycle arrest and apoptosis of cancer cells. Also, the common cell cycle inhibiting protein, p27, and the new cell cycle regulator, Cdk5, are involved in retinoic acid’s effects. These results provide new evidence indicating that the molecular mechanisms of/in retinoic acid may control cancer cells’ fates. Since high doses of retinoic acid may lead to cytotoxicity, it is probably best utilized as a potential supplement in one’s daily diet to prevent or suppress cancer progression. In this review, we have collected numerous references demonstrating the findings of retinoic acid in melanoma, hepatoma, lung cancer, breast cancer, and prostate cancer. We hope these observations will shed light on the future investigation of retinoic acid in cancer prevention and therapy.
Mei-Chih Chen; Shih-Lan Hsu; Ho Lin; Tsung-Ying Yang. Retinoic acid and cancer treatment. BioMedicine 2014, 4, 22 .
AMA StyleMei-Chih Chen, Shih-Lan Hsu, Ho Lin, Tsung-Ying Yang. Retinoic acid and cancer treatment. BioMedicine. 2014; 4 (4):22.
Chicago/Turabian StyleMei-Chih Chen; Shih-Lan Hsu; Ho Lin; Tsung-Ying Yang. 2014. "Retinoic acid and cancer treatment." BioMedicine 4, no. 4: 22.
We greatly appreciate the interest expressed in the letter regarding the enhancement of chemo- or radiosensitivity by inhibition of clusterin (CLU) expression in a number of solid tumors. There are at least two pathways that are simultaneously altered when secretory clusterin (sCLU) is targeted by antisense oligonucleotide (ASO) or siRNA. One involves the upregulation of chemo- or radiosensitivity. Another involves downregulation of metastasis. In the case of prostate cancer, since the expression of sCLU is correlated with androgen ablation, anti-clusterin therapy with OGX-011 has been demonstrated to benefit patients by overcoming sCLU-associated chemoresistance [6]. In our reported data, inhibition of sCLU expression in sCLU-rich NSCLC cells resulted in high chemosensitivity [2]. Other reports have shown similar effects in other low sCLU expressing lung cancer cells [1, 5]. Therefore, upregulated chemosensitivity can be achieved by sCLU inhibition, independent of sCLU level in cancer
Ching-Yuan Cheng; Shur-Hueih Cherng; Wen-Jun Wu; Tsung-Ying Yang; Xin-Yi Huang; Fu-Tien Liao; Ming-Fang Wu; Gwo-Tarng Sheu. Reply to: Clusterin inhibition to enhance tumor chemosensitivity in systemic tumors. Cancer Chemotherapy and Pharmacology 2013, 71, 1103 -1104.
AMA StyleChing-Yuan Cheng, Shur-Hueih Cherng, Wen-Jun Wu, Tsung-Ying Yang, Xin-Yi Huang, Fu-Tien Liao, Ming-Fang Wu, Gwo-Tarng Sheu. Reply to: Clusterin inhibition to enhance tumor chemosensitivity in systemic tumors. Cancer Chemotherapy and Pharmacology. 2013; 71 (4):1103-1104.
Chicago/Turabian StyleChing-Yuan Cheng; Shur-Hueih Cherng; Wen-Jun Wu; Tsung-Ying Yang; Xin-Yi Huang; Fu-Tien Liao; Ming-Fang Wu; Gwo-Tarng Sheu. 2013. "Reply to: Clusterin inhibition to enhance tumor chemosensitivity in systemic tumors." Cancer Chemotherapy and Pharmacology 71, no. 4: 1103-1104.
In terms of drug resistance, cancer cells usually benefit from high clusterin (CLU) expression on chemotherapy. In contrast, CLU expression has been found to be a favorable prognostic factor in lung cancer patients. The aims of this study are to determine the association between CLU expression and chemotherapeutic sensitivity and the potential role of CLU in migration in human non-small-cell lung cancer (NSCLC) cell lines. The levels of clusterin in NSCLC cell lines were altered by short hairpin RNA interference (shRNAi) and overexpression on chemosensitivity assay. Migratory ability of these cell lines was also investigated. H1355 cells with the highest level of CLU demonstrated the lowest sensitivities to Adriamycin (ADR), docetaxel (DOC), and gemcitabine (GEM) treatment. Inhibition of CLU expression in H1355 cells resulted in higher chemosensitivities. When CLU was stably overexpressed in A549 and H1299 cells, only the chemosensitivity to ADR was reduced. The migratory ability of CLU-overexpressing cells significantly decreased. Moreover, MMP2 transcription was inhibited in CLU-overexpressing H1299 cells. These results indicated lower metastatic potential for cancer cells with high CLU level. Lung cancer cells with high level of CLU have reduced chemosensitivity. High level of CLU may result in migratory inhibition and thus favorable prognosis in lung cancer.
Ching-Yuan Cheng; Shur-Hueih Cherng; Wen-Jun Wu; Tsung-Ying Yang; Xin-Yi Huang; Fu-Tien Liao; Ming-Fang Wu; Gwo-Tarng Sheu. Regulation of chemosensitivity and migration by clusterin in non-small cell lung cancer cells. Cancer Chemotherapy and Pharmacology 2011, 69, 145 -154.
AMA StyleChing-Yuan Cheng, Shur-Hueih Cherng, Wen-Jun Wu, Tsung-Ying Yang, Xin-Yi Huang, Fu-Tien Liao, Ming-Fang Wu, Gwo-Tarng Sheu. Regulation of chemosensitivity and migration by clusterin in non-small cell lung cancer cells. Cancer Chemotherapy and Pharmacology. 2011; 69 (1):145-154.
Chicago/Turabian StyleChing-Yuan Cheng; Shur-Hueih Cherng; Wen-Jun Wu; Tsung-Ying Yang; Xin-Yi Huang; Fu-Tien Liao; Ming-Fang Wu; Gwo-Tarng Sheu. 2011. "Regulation of chemosensitivity and migration by clusterin in non-small cell lung cancer cells." Cancer Chemotherapy and Pharmacology 69, no. 1: 145-154.