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Delta-actitoxin-Avd1a binds OTUD6B. 609 / 609
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"NRIR in monocytes of patients with SSc was closely related to IFN response, which further supports the abnormal phenomenon of IFN in SSc. xref Abd-Elmawla et al analyzed the plasma expression profile of lncRNA, and studied its relationship with disease types and related clinical indicators, and proposed plasma SPRY4-IT1, HOTTIP, ANCR and TINCR as new candidate biomarkers for SSc. xref Further, the study by Takata et al unveiled that OTUD6B-AS1 regulated cell proliferation and apoptosis through the expression of cyclinD1 independent of the sense gene, revealing its potential value in regulating the apoptosis of fibroblasts and vascular smooth muscle cells, and may participate in the pathogenesis of SSc. xref Another study by Pachera et al showed that the expression of H19X was dose-dependent with the concentration of TGF-β and could effectively induce fibroblast differentiation and survival, enhance ECM production and tissue progressive fibrosis. xref Of note, the study by Wang et al demonstrated that intrinsic TGF-β activation may result in increased expression of TSIX in the serum of patients with SSc, and that TSIX was able to regulate collagen production. xref Since increased levels of TSIX appear to correlate with levels of skin fibrosis, it has the potential to act as a novel disease biomarker that may also serve as a potential therapeutic target. xref Recently, HOTAIR was found to induce skin fibroblasts differentiation in vitro, driving EZH2-dependent myofibroblast activation in SSc through miRNA 34a-dependent activation of NOTC H. xref Apart from Notch signaling, HOTAIR can also induce fibrosis through Hedgehog signaling. xref The differentially expressed ncRNA00201 and PSMB8-AS1 in blood and MGC12916 in fibroblasts were also confirmed to be important players in the pathogenesis of SSc. xref , xref , xref The involvement of lncRNAs in the pathogenesis of scleroderma is intricate and complicated, which may be through the epigenetic regulation of the gene itself, interacting with miRNAs, or affecting the secretion of important cytokines such as IL-6 and TNFα, xref and participating in regulating the expression of fibrosis-related genes."
sparser
"As shown in the forest map, AC108449.2, AC098484.1, AC092611.2, AC234775.3, OTUD6B-AS1, SPINT1-AS1 and AC007637.1 are considered a protective element, but LINC-PINT, ANKRD10-IT1, ITGB2-AS1, AC021078.1, AC127024.4, AC009120.2, AC090589.3, AC087481.3, LINC01004, AC008105.3, INE1, AC048382.2, AC012170.2, AP002807.1, THUMPD3-AS1, DLEU2, AC069281.2 and AC008870.2 were detrimental parts ( xref )."
sparser
"Hsa-miR-21-5p, which is closely related to KLF9, was highly expressed in tumors and KIRC patients with high expression of hsa-miR-21-5p have a worse prognosis, suggesting that a negative regulatory relationship between KFL9 and hsa-miR-21-5p and that hsa-miR-21-5p influenced the malignant progression of tumors. ( xref ) Moreover, we further identified four upstream lncRNA targets OTUD6B-AS1, AL162377.1, AC108449.2, and AF111167.2 in StarBase (the inclusion criteria here were the absolute value of correlation coefficient > 0.3 and P < 0.05). ( xref ) They were all closely related to hsa-miR-21-5p. ( xref ) The prognosis of KIRC patients with their high expression levels was better. ( xref ) Therefore, we speculated that there was a negative regulatory relationship between lncRNAs and miRNA."
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"Among the nine key cuproptosis-related lncRNAs we obtained, MME-AS1 has been confirmed to be related to the survival in intrahepatic cholangiocarcinoma [ xref ], while OTUD6B-AS1 is not only associated the progression of various cancers, but also with tumor drugs resistance [ xref – xref ]."
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"Multivariate Cox regression identified 8 lncRNAs with the best predictive correlation: AL122010.1, OTUD6B-AS1, EGOT, AP005131.2, Z68871.1, AC024361.1, LINC00987, ST7-AS1 ( xref ), and we further visualized the correlation between lncRNAs and mRNAs using Cytoscape ( xref ), showing that Z68871.1, AP005131.2 and AC024361.1 were most closely associated with mRNAs."
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"We used the RS = (0.542214503 × Z68871.1 expression) + (0.571403384 × OTUD6B-AS1 expression) - (0.8962291962× AC024361.1 expression) - (0.576665716 × LINC0098 expression) - (0.76381661 × AL122010.1 expression) - (0.717527719 × ST7-AS1 expression) - (0.497395506 × AP005131.2 expression) - (0.411082836 × EGO expression) to calculate the score of each patient."
sparser
"We found that similar to the multifactorial results, high expression levels of AC024361.1, LINC00987, AL122010.1, EGOT, ST7-AS1, and AP005131.2 were correlated with a better prognosis; on the contrary, high expression levels of OTUD6B-AS1 and Z68871.1 were associated with a poor prognosis of patients."
sparser
"A total of 8 immune-related lncRNAs were obtained, including OTUD6B-AS1(HR = 1.698; 95% CI 1.066–2.707, p = 0.026), AL122010.1(HR = 0.404; 95% CI 0.209–0.782, p = 0.007), AC136475.2(HR = 0.596; 95% CI 0.369–0.964, p = 0.035), AL161646.1(HR = 1.215; 95% CI 0.954–1.549, p = 0.115), AC245297.3(HR = 0.710;95% CI 0.450–1.121, p = 0.142), LINC00578(HR = 1.269; 95% CI 1.001–1.609, p = 0.049), LINC01871(HR = 0.657; 95% CI 0.448–0.964, p = 0.032), AP000442.2 (HR = 0.335; 95% CI 0.101–1.115, p = 0.075) (Fig. xref d, Table xref )."
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"Previous reports indicated that high expression of hsa-miR-21-5p in six cancers including KIRC was strongly associated with shorter overall survival, which was consistent with our results. xref , xref In addition, hsa-miR-21-5p could drive T helper cells to participate in the kidney function and progression of IgA nephropathy. xref Wang et al xref found that high expression of LncRNA OTUD6B-AS1 represented a favorable prognosis and inhibited the proliferation and progression in KIRC."
sparser
"Eleven out of 23 lncRNAs including MAPKAPK5-AS1, TRIM52-AS1, CRYZL2P, RNF216P1, CD63-AS1, WAC-AS1, PMS2P1, Alu-mediated p21 transcriptional regulator (APTR), ARRDC1-AS1, PPIAP22, and HEIH were related to HCC, whereas the FCF1P2, OTUD6B-AS1, and MHENCR were related to osteosarcoma, renal cancer, and melanoma, respectively."
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"The risk score was determined through the application of the multivariate Cox regression formula as follows: risk score = MIR4435-2HG × (0.867022528575273) + EGOT × (-0.235669144798444) + ST7-AS1 × (-1.11551827892176) + PDCD6IP-DT × (− 0.750754400726742) + ERICH6-AS1 × (− 1.20438658732549) + LINC00310 × (0.882320522314723) + OTUD6B-AS1 × (0.423845118028363) + LINC01871 × (− 0.415778456572796)."
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"lncRNA has a prominent regulatory role in the Wnt-β-catenin pathway: The increased expression of MSC-AS1 , FAST , JPX , and LALR1 directly or indirectly enhances the stability of β-catenin, thereby activating the Wnt-β-catenin pathway ( xref , xref ); meanwhile, the decreased expression of OTUD6B-AS1 indirectly activates the Wnt-β-catenin pathway ( xref )."
sparser
"By performing univariate Cox regression analysis on the training set, we identified 13 PRLS (OTUD6B-AS1, AL353622.1, LINC02035, HM13-IT1, FIRRE, NORAD, AC010980.2, AL133243.2, NNT-AS1, PAX8-AS1, POC1B-AS1, U47924.3, and ATP6V0E2-AS1) that had potential prognosis value for UCEC ( xref )."
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"The overexpression of long non-coding RNA ovarian tumor domain-containing 6B-antisense RNA1 (lncRNA OTUD6B-AS1) stabilizes the tripartite motif 16 (TRIM16) mRNA by binding to the RNA-binding protein human antigen R and increases TRIM16 mRNA levels, promoting GPX4-mediated ferroptosis and inhibiting radioresistance in CRC cells; however, inhibiting ferroptosis attenuates the inhibitory effect of overexpressed lncRNA OTUD6B-AS1 in CRC radioresistance xref ."
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"Sixteen lncRNAs (ACTA2-AS1, CARD8-AS1, HCP5, HHIP-AS1, HOTAIRM1, ITGB2-AS1, LINC00324, LINC00605, LINC01503, LINC01547, MIR31HG, MIR155HG, OTUD6B-AS1, PSPXD2A1, SH3PMG3-AS1, SH3, and ZBED5-AS1) were found to be significantly correlated with the OS rate of patients with ovarian cancer (OC) [ xref ]."
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"Western blotting showed that, under lncRNA OTUD6B-AS1 overexpression and As 2 O 3 treatment (20 μ mol/L), the expression of Bax and Caspase3 was significantly increased, while levels of Bcl-2 were significantly decreased relative to lncRNA OTUD6B-AS1 overexpression or As 2 O 3 treatment ( P < 0.01; Figures xref – xref )."
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"Xenograft tumors with both lncRNA OTUD6B-AS1 overexpression and As 2 O 3 treatment showed significantly weaker Ki-67 expression ( xref ) and significantly stronger p57 expression ( xref ), compared with xenograft tumors with lncRNA OTUD6B-AS1 overexpression or As 2 O 3 treatment alone."
sparser
"Interestingly, following lncRNA OTUD6B-AS1 overexpression, levels of ROS and MDA in T24 cells treated with As 2 O 3 were significantly enhanced ( P < 0.01); however, the activities of the antioxidant enzymes SOD and GSH-Px showed the opposite trend, suggesting an impaired antioxidant defense system (Figures xref and xref )."
sparser
"To corroborate these findings, we conducted ChIP assays and found that the pull-down with the MTF1 antibody greatly enriched the lncRNA OTUD6B-AS1 promoter region containing putative metal response elements (nucleotides 754 to 854 in the promoter) by almost 5.20-fold relative to control IgG ( P < 0.01), and a reference region (nucleotides 100 to 200 in the promoter) without putative MRE was used as a negative control ( xref ."
sparser
"Here, we found that lncRNA OTUD6B-AS1 transcription was activated by As 2 O 3 in bladder cancer cells, and these results were validated using a xenograft tumor model, suggesting that the antitumor effects of As 2 O 3 may be via upregulation of lncRNA OTUD6B-AS1; however, the roles of lncRNA OTUD6B-AS1 in exacerbated As 2 O 3 -induced oxidative damage have yet to be elucidated."
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"Ectopic expression of OTUD6B-AS1 inhibits tumor cell migration and invasion through suppressing the Wnt/β-catenin axis and reducing the expression of epithelial-to-mesenchymal transition (EMT)-related proteins including E-cadherin, N-cadherin, and Snail (Wang et al., 2019[ xref ])."
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"Long noncoding RNAs (lncRNAs) are loosely defined as RNAs that exceed 200 bases in length and have no apparent coding capacity, which have been shown to have important roles in promoting tumor formation and progression. [ xref , xref ] Currently, only few lncRNAs have recently been reported to be implicated in the modulation of autophagy in TNBC cells. [ xref ] For example, NAMPT‐AS is an oncogenic lncRNA in TNBC that epigenetically activates NAMPT to promote tumor progression and metastasis. [ xref ] Moreover, lncRNA OTUD6B‐AS1 promotes paclitaxel resistance in TNBC by regulation of miR‐26a‐5p/MTDH pathway‐mediated autophagy. [ xref ] As only a few autophagy‐associated lncRNAs were discovered in TNBC, the landscape of lncRNAs dysregulated and their molecular mechanisms in autophagic regulatory networks in TNBC remain largely unknown."
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"Using these HRLs, we finally constructed a novel prognostic model for patients with breast cancer, which consisted of 12 PHRLs: TDRKH-AS1, AC011978.2, AC110995.1, OTUD6B-AS1, YTHDF3-AS1, AL512380.1, MIR4435-2HG, HSD11B1-AS1, LINC02084, TRG-AS1, AL451085.3, and AL109955.1 (RBM38-AS1)."
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"Lentivirus-mediated overexpression of OTUD6B-AS1 significantly reduces cell proliferation and promotes cell apoptosis in clear cell renal cell carcinoma (ccRCC), while OTUD6B-AS1 overexpression of β-catenin reduces the activity of the Wnt/β-catenin pathway and partially inhibits cell migration and invasion [ xref ]."
sparser
"Finally, OTUD6B also plays an important role in several diseases other than tumors; for example, biallelic variants in OTUD6B lead to mental retardation syndromes associated with seizures and dysmorphic features [ xref ]; OTUD6B-AS1 is also a key regulator of apoptosis in systemic sclerosis [ xref ]."
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"Long non-coding RNAs (lncRNAs) exert a key role in multiple cellular processes such as cell proliferation, migration and chemoresistance. xref , xref Du et al . found that lncRNA DLX6-AS1 enhanced cisplatin resistance in TNBC cells via miR-199b- 5p/PXN signaling. xref Li et al . showed that lncRNA OTUD6B-AS1 facilitate paclitaxel resistance in TNBC via miR-26a-5p/MTDH axis. xref Additionally, evidence has reported that lncRNAs play a key function in intracellular communication as well as in the tumor microenvironment. xref , xref "
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"The main regulation mechanisms and results of the JAK/STAT signaling pathway include FUS-dependent JAK/STAT3 pathway activation (ITIH4-AS1), miR-18a/STAT3 sponging (CASC2), apoptosis induction via STAT5 and STAT6 (RP11-468E2.5), apoptosis induction via targeting STAT5/6 (RP11-468E2.5), CRC development via miR-9-5p/STMN1 and IL-6R regulation (lncRNA LINC01116), JAK/STAT3 pathway downregulation, expression of E-cadherin and occludin (lncRNA AB073614), cell proliferation and inhibition of apoptosis, JAK1/STAT3 signaling inhibition, Bcl-2 increase, caspase-3 and Bax downregulation (lncRNA LINC00346), miR-21-5p sponging, PNRC2 regulation, CRC progression inhibition (lncRNA OTUD6B-AS1), CRC development via miR-9-5p/STMN1 and IL-6R regulation (LINC01116), TPT1-mediated FAK and JAK-STAT3 signaling upregulation, CRC cell migration, miR-149-3p sponging, and CRC progression and metastasis (RNA TPT1-AS1 and RNA HOXA11-AS) ( xref )."
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"Other lncRNAs identified as potentially involved in cancer include FRMD6-AS1 [ xref , xref ] and LINC00466 [ xref , xref ], which have also been shown to promote tumor growth in vivo alongside [ xref ] LINC00877 [ xref ], LINC01091 [ xref ], NNT-AS1 [ xref , xref , xref ], ZNF252P-AS1 [ xref ], LZTS1-AS1 [ xref ], and OTUD6B-AS1 [ xref , xref ]."
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"Although several publications have indicated the occurrence of necroptosis regulators in KIRC, very few data are available on the involvement of lncRNAs in controlling or decreasing the neurotrophic signaling in kidney cancer, in particular based on OTUD6B-AS1, AL162377.1, AC108449.2, AF111167.2, and hsa-miR-21-5p targeting KLF9 [ xref – xref ]."
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"The role of OTUD6B-AS1 in different cancers varies: for example, over-expression of OTUD6B-AS1 in kidney cancer acts on the wnt/β-catenin pathway to inhibit cancer development and metastasis xref ; OTUD6B-AS1 is a biomarker of ovarian cancer occurrence and prognosis xref , and high expression of OTUD6B‐AS1 is closely associated with poor prognosis of ovarian cancer xref ."
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"We calculated the risk scores for all samples using the following formula: Risk score = (0.309031851 × Exp of TDRKH-AS1) + (0.213481355 × Exp of AC011978.2) + (0.170772984 × Exp of AC110995.1) + (0.051734285 × Exp of OTUD6B-AS1) + (0.046646469 ×Exp of YTHDF3-AS1) + (0.019875191 × Exp of AL512380.1) + (0.019087737 × Exp of MIR4435-2HG) + (–0.037067764 × Exp of HSD11B1-AS1) + (–0.063799579 × Exp of LINC02084) + (–0.162152639 × Exp of TRG-AS1) + (–0.399031951 × Exp of AL451085.3) + (–0.886350422 × Exp of AL109955.1)."
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"Univariate Cox regression analysis was used for selecting six lncRNAs (NIFK-AS1, TP53TG1, TOLLIP-AS1, YTHDF3-AS1, LINC00839, and OTUD6B-AS1) that were associated with the prognosis of patients with BC ( xref ). xref depicts a forest map of the univariate Cox regression analysis."
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"In this study, we constructed a risk model for the ARG-related lncRNAs NRAV, MCM3AP-AS1, OTUD6B-AS1, AC026356.1, AC009133.1, DDX11-AS1, AC108463.2, MIR4435-2HG, WARS2-AS1, LINC01094, and HCG18 and examined the relationship between the model and the prognosis and immune cells of patients with HCC."
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"The Wnt/β-catenin pathway is evolutionarily well-conserved, and aberrant activation of this pathway can cause abnormal cell growth and malignant transformation ( xref ; xref ). xref revealed that the novel lncRNA OTUD6B-AS1 decreased the activity of the Wnt/β-catenin pathway and suppressed the expression of EMT-related proteins."
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"In this study, we found that the expression of the lncRNA OTUD6B-AS1 was downregulated in ccRCC tissue samples and that patients with low OTUD6B-AS1 expression had shorter overall survival than patients with high OTUD6B-AS1 expression, which showed that the different expression level of OTUD6B-AS1 indirectly correlated with survival of patients."
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"After the LASSO regression, 11 of them, including AL023882.1, AC091588.1, AC138028.2, AC027514.1, AL592301.1, LRRC8C-DT, MFF-DT, NIFK-AS1, MECOM-AS1, OTUD6B-AS1, and RNF32-AS1 were selected to develop a risk score system, which was subsequently proven to have an independent prognostic value."
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"Then, Kaplan-Meier analysis was used to evaluate the relationship between OTUD6B-AS1 expression in ccRCC and patient clinicopathological characteristics, and the results showed that the survival time of the patients with pathologic stage I + II disease ( n = 318) was longer than that of the patients with advanced stage lesions ( n = 205) ( P < 0.0001, Additional file xref : Figure S1A)."
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"To explore the role of the lncRNA OTUD6B-AS1 in ccRCC, we analyzed the expression of OTUD6B-AS1 in a cohort of 75 ccRCC tissue samples and matched nontumor samples using qRT-PCR analysis, with our results showing that OTUD6B-AS1 expression was remarkably decreased in the ccRCC tissue samples compared with the paired adjacent normal tissue samples (Fig. xref a and b)."
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"Then, we included the variables age, gender, clinical tumor grade, pathologic stage, lymph node status, metastasis status, and OTUD6B-AS1 mRNA level in a multivariate Cox regression model and found that the OTUD6B-AS1 mRNA level was an independent predictor for overall survival status in KIRC patients (HR = 0.275, 95% CI 0.081–0.930, p = 0.038; Table xref )."
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"Univariate Cox analysis ( p < 0.05) was utilized to choose 81 differentially expressed prognostic-related lncRNAs: THBS4-AS1, LINC01711, MACORIS, KIAA1671-AS1, BACE1-AS, SIAH2-AS1, LINC00571, RAP2C-AS1, ARF4-AS1, MYOSLID, PLBD1-AS1, FALEC, GNG12-AS1, AGAP2-AS1, OXCT1-AS1, FOXD2-AS1, SNHG9, LINC00882, APCDD1L-DT, SNHG11, OXCT1-AS1, CTBP1-DT, HHLA3, NNT-AS1, MAP3K4-AS1, OIP5-AS1, LINC01671, LASTR, NFE4, GTF3C2-AS1, LINC01801, LINC00886, CDK6-AS1, EIF3J-DT, MHENCR, LINC01605, H1-10-AS1, SBF2-AS1, PCCA-DT, LYPLAL1-DT, COLCA1, SNHG3, GAS6-DT, LINC02027, SGMS1-AS1, BDNF-AS, KLHL7-DT, NORAD, DHRS4-AS1, SNHG15, LHFPL3-AS2, LINC00460, LINC02446, LINC02195, LINC00271, GATA2-AS1, LINC01011, SEPTIN7-DT, SNHG8, UGDH-AS1, CYTOR, MANCR, MIR4435-2HG, ITGA9-AS1, ZBTB20-AS4, SUCLG2-AS1, LINC01507, OTUD6B-AS1, EIF1B- AS1, HCG25, PAXIP1-AS2, WDFY3-AS2, TGFB2-AS1, BAALC-AS1, LINC00941, LINC02154, SNHG6, EMS2OS, MINCR, ATP1A1-AS1, LINC00623, and LINC01415 ( xref )."
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"A total of 14 lncRNAs were identified as protective genes (AC022150.4, AC061992.1, AC090948.3, AC092794.1, AC107464.3, AL021707.8, AL451085.2, AL606834.2, FLJ42351, LINC00926, LINC01871, TNFRSF14−AS1, U73166.1 and USP30−AS1) with HRs < 1 while 10 lncRNAs (AC022150.2, AC090948.1, AC243960.1, AL021707.6, ITGB2−AS1, OTUD6B−AS1, SP2−AS1, TOLLIP−AS1, Z68871.1 and ZNF337−AS1) were associated with increased risk with HRs >1."
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"OTUD6B‐AS1 suppresses viability, migration and invasion in thyroid carcinomas, colorectal cancer cell and renal cell carcinoma. xref , xref , xref , xref On the other hand, OTUD6B‐AS1 promotes hepatocellular carcinoma cells proliferation and invasion and induces chemoresistance in breast cancer cell and cervical cancer cell. xref , xref , xref How to make a wide use of OTUD6B‐AS1 is worth exploring and may provide a novel strategy to cancer treatment."
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"Additionally, 12-FRLncRNA signature involved with LINC01871, LINC00393, AC121247.2, LINC02384, LIPE-AS1, HSD11B1-AS1, AC010655.2, LINC01419, PTPRD-AS1, AC099329.2, OTUD6B-AS1, and LINC02266 could accurately predict the prognosis of patients with BC, which was confirmed by the training set, validation set, and set from GEO database."
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"The upregulation of OTUD6B-AS1 expression significantly upregulated the expression of the epithelial marker E-cadherin, while the expression levels of the mesenchymal cell markers N-cadherin and Snail were downregulated in both the ACHN and OS-RC-2 cells with enhanced expression of OTUD6B-AS1 (Fig. xref c)."
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"A prognostic risk model comprised of six m 6 A-regulated lncRNAs-Z68871.1, AL122010.1, AL138724.1,OTUD6B-AS1, AC090948.3 and eosinophil granule ontogeny transcript (EGOT) for high-risk patients with tumor-infiltrating immune cells, indicated that m 6 A-regulated lncRNAs may modulate the immune microenvironment in breast cancer ( xref )."
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"The risk score for each patient was calculated by the formula: risk score = (1.14515Expr PPIC-AS1) + (−1.94235Expr MME-AS1) + (−0.54517Expr AC012676.3) + (1.246856Expr MFF-DT) + (0.83774Expr OTUD6B-AS1) + (−0.49163Expr AL109936.9) + (−0.87639Expr AL807757.2) + (−1.34052Expr AL118556.1) + (−2.04930Expr AL137847.1)."
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"In a series of assays, it was observed that the additional treatment with miR-3171 mimics following OTUD6B-AS1 overexpression in HCT116 cells promoted the proliferation, invasion and migration of HCT116 cells, suggesting that OTUD6B-AS1 overexpression inhibited the proliferation, invasion and migration of HCT116 cells via downregulation of miR-3171 expression."
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"In conclusion, to the best of our knowledge, the present study was the first to investigate the role of OTUD6B-AS1 in CRC cells, and to reveal that lncRNA OTUD6B-AS1 overexpression inhibited the proliferation, invasion and migration of HCT116 cells, at least partially, by targeting miR-3171."
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"In the field of cancer research, Wang and colleague reported OTUD6B-AS1 was downregulated in ccRCC tissue samples, and that patients with low OTUD6B-AS1 expression had shorter overall survival than patients with high OTUD6B-AS1 expression, which showed that the different expression levels of OTUD6B-AS1 indirectly correlated with patient survival ( xref )."
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"The results of qRT-PCR analyses showed that lncRNA OTUD6B-AS1 levels in T24 bladder cancer cells were significantly and dose-dependently increased in response to As 2 O 3 ; lncRNA OTUD6B-AS1 levels were increased by more than 8.65-fold by As 2 O 3 treatment at 20 μ mol/L for 6 h, relative to untreated T24 cells ( P < 0.01) ( xref )."