In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Context: Urothelial carcinoma associated 1 (UCA1) functions as an oncogene, which promotes cancer cell proliferation, invasion, and metastasis, and is responsible for drug resistance. This study aimed to determine the expression level of UCA1 in ovarian cancer and to further investigate its clinical significance.', 'The expression levels of UCA1 in ovarian cancer and normal ovaries were determined by quantitative real-time PCR. The relationship between UCA1 expression and clinical features and the prognostic value of UCA1 for overall survival were examined.', 'UCA1 expression in ovarian cancer tissues was significantly upregulated compared with normal ovarian tissues. High UCA1 expression was related to lymph node metastasis, FIGO stage, and response to chemotherapy. Kaplan-Meier analysis demonstrated that high UCA1 expression was associated with poorer overall survival in patients with ovarian cancer. Cox proportional hazards analysis showed that high UCA1 expression was an independent prognostic marker of poor outcome. This effect remained significant in the further stratification analysis.\Question: Does uCA1 overexpression predict clinical outcome of patients with ovarian cancer receiving adjuvant chemotherapy?
Our findings provided the first evidence that UCA1 may serve as an indicator of response to chemotherapy and prognosis of ovarian cancer. UCA1 may play an important role in the progression of ovarian cancer.

Context: Hypoxia is associated with human non-small cell lung cancers (NSCLC), which are highly resistant to chemotherapy. The hypoxia inducible factor (HIF) as a transcription factor in response to hypoxia indicates that it could be a novel, tumor-specific target for anticancer therapy. We hypothesized that disruption of HIF pathway through lentiviral vector-mediated HIF-1alpha RNA interference (RNAi) could reverse the hypoxia-induced resistance to chemotherapy.', 'We transfected Human NSCLC cell lines, SPCA1 and A549 with HIF-1alpha specific RNAi lentiviral vectors as well as controls. HIF-1alpha silenced cells [SPCA1/HIF-1alpha(-) and A549/HIF-1alpha(-)] were screened by blasticidin. They were incubated in 19 or 0.5% O2 for 16 h followed by the assessment of chemosensitivity to cisplatin and doxorubicin with MTT and clonogenic assays. Quantitative RT-PCR and Western blot analysis were used to detect the expressions of HIF-1alpha mRNA and protein, respectively. Moreover, flow cytometry was used to monitor the expression of P-glycoprotein.', 'Exposure of SPCA1 and A549 cells to 0.5% O2 significantly increased resistance to cisplatin and doxorubicin, in contrast to cells incubated in normoxia. Transduction of SPCA1 with HIF-1alpha RNAi vector resulted in sequence specific silencing with 87.2 and 84.6% decreases of HIF-1alpha mRNA transcription and 97.3 and 94.8% of protein expressions in normoxia and hypoxia, respectively. Correspondingly, they are 89.2, 89.9% and 97.2, 88.4% decreases in A549 cells. Hypoxia-induced resistance to cisplatin and doxorubicin were reversed in SPCA1/HIF-1alpha(-) and A549/HIF-1alpha(-) cells. There was no significant P-glycoprotein increase induced by hypoxia in NSCLC cells.\Question: Is hypoxia-induced resistance to cisplatin and doxorubicin in non-small cell lung cancer inhibited by silencing of HIF-1alpha gene?
Our studies demonstrated that hypoxia-induced chemoresistance to cisplatin and doxorubicin in NSCLC cells is through the HIF pathway. MDR1 regulation may not be involved in hypoxia-induced chemoresistance. Combining delivery of HIF-1alpha RNAi lentiviral vector with cisplatin-related chemotherapy regimens may enable us to develop more effective strategy for NSCLC therapy.

Context: Stricture formation in Crohn's disease (CD) occurs as a result of persistent intestinal inflammatory activation, which leads to enhanced adhesion molecule expression in serosal fibroblasts (SFs). Vasoactive intestinal peptide (VIP) has anti-inflammatory and immunoregulatory properties. Treatment with VIP prevents experimental CD in animal models at the clinical and pathologic levels. The present study reports the effect of VIP on the expression of intracellular adhesion molecule-1 (ICAM-1) in IL-1beta-stimulated human colon SFs.", 'Primary human colon SFs were incubated with or without IL-1beta (10 ng/mL) in the presence or absence of VIP at various concentrations (0.1 to 100 nM) for designated time. Cell surface and cytosolic ICAM-1 expression were evaluated by flow cytometry and Western blot analysis, respectively. The DNA binding capacity of NF-kappaB was analyzed by electrophoretic mobility shift assay. The phosphorylation of IkappaB-alpha was examined by Western blot analysis.', 'VIP inhibited IL-1beta-induced expression of ICAM-1 in a dose-dependent manner. The IL-1beta-induced ICAM-1 was also inhibited by a potent inhibitor of NF-kappaB, MG132. VIP also decreased IL-1beta-induced NF-kappaB DNA binding capacity and phosphorylation of IkappaB-alpha.\Question: Does vasoactive intestinal peptide inhibit adhesion molecule expression in activated human colon serosal fibroblasts by preventing NF-kappaB activation?

VIP has an inhibitory effect on IL-1beta-induced ICAM-1 expression in SFs, which may be associated with NF-kappaB activity. This may make VIP potentially a novel therapeutic agent for preventing stricture formation in Crohn's disease.