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There exists some cognitive bias in the study on the court tea utensils of the early Ming Dynasty, due to the influence of connoisseurship books and tea books in late Ming Dynasty. Description on the court tea utensils of the early Ming Dynasty in those connoisseurship books and tea books reflect the selective preference for the literati’s aesthetics of that time, which can not reveal the historical facts of the court tea ware in early Ming Dynasty. On the basis of reflecting on the late Ming literati's discourse, combined with documentary records and archaeological excavations related to the court, it is believed that the high footed cup is one of the types of tea ware, used with the teapot with almond-shaped body and teapot with the shape of monk’s hat. Combined with large teapots, tea cups of the same proportion as the high-footed cups, around 15 cm in diameter, may also be one of the types of tea ware used in the court of early Ming Dynasty. The size is far bigger than those ones preferred by the late Ming literati. [ABSTRACT FROM AUTHOR]

Objective To explore the function and mechanism of long non-coding RNA MIR503HG in esophageal squamous cell carcinoma (ESCC). Methods The MIR503HG expression data in 60, 119 and 23 cases of ESCC and their paired adjacent tissues were chosen from three ESCC datasets GSE53622, GSE53624 and GSE130078, respectively. The expression data of MIR503HG in 81 ESCC tissues and 271 unpaired normal esophageal tissues were screened from the combined dataset of Cancer Genome Atlas and Genotype-Tissue Expression Database ( TCGA + GTEx ). The MIR503HG knockdown plasmid was constructed, packaged into lentivirus. The lentivirus was used to infect with esophageal squamous cell carcinoma cell lines KYSE30 and KYSE510 to screen out the stable MIR503HG knockdown cell lines. ESCC cell line KYSE30 was transiently transfected with miRNA mimics to overexpress hsa-miR-503-3p and hsa- miR-503-5p.The expression levels of MIR503HG, hsa-miR-503-3p and hsa-miR-503-5p were detected by quantitative real-time polymerase chain reaction. The proliferation ability of the cells was detected by cell counting kit 8 and clone formation assay. The invasion and migration ability of the cells were detected by Transwell assay. Cell cycle was detected by flow cytometry. The effect of MIR503HG on the proliferation of ESCC was detected by xenograft experiment in BALB/ c-nu / nu mice. Results Both GEO and TCGA+GTEx databases showed that the expression of MIR503HG in ESCC tissues was higher than that in adjacent tissues and normal esophageal tissues (P<0.01). Compared with shNC group, the proliferation rates of KYSE30 and KYSE510 cells after knockdown of MIR503HGwere significantly inhibited (P<0.001). The colony formation numbers of KYSE30 cells in shMIR503HG1 group and shMIR503HG2 group were (2.00±1.41) and (1.33± 0. 47), respectively, significantly lower than that of the shNC group ( P = 0. 002). The clone formation numbers of KYSE510 cells in shMIR503HG1 group and shMIR503HG2 group were ( 174.67± 15.97) and (80.33±6. 34), respectively, significantly lower than that of the shNC group ( P< 0. 001). The invasive numbers of KYSE30 cells in shMIR503HG1 group and shMIR503HG2 group were 75.33±6.02 and 45.67± 7.59, significantly lower than that of the shNC group(P<0.001). The migrating number of KYSE30 cells in shMIR503HG1 group and shMIR503HG2 group were 244.00±10.23 and 210.67±13.52, significantly lower than that of the shNC group(P< 0.001), and the cell cycle was arrested in G0/G1 phase. The xenograft experiment showed that the subcutaneous tumor in shMIR503HG group was significantly smaller than that in shNC group, and the tumor weight in shMIR503HG group was ( 0.097± 0.026) g, which was lower than (0.166±0.021) g in shNC group (P<0.001). After knockdown of MIR503HG, the relative expression levels of hsa-miR-503-3p in KYSE30 cells of shMIR503HG1 group and shMIR503HG2 group were 0.66±0.02 and 0.58±0.00, respectively, the relative expression levels of hsa-miR-503-5p were 0.64±0.00 and 0.68±0.03, respectively, which were all lower than those in shNC group (P<0.01). After knockdown of MIR503HG, overexpression of hsa-miR-503-3p and hsa-miR-503-5p attenuated the inhibitory effects of knockdown of MIR503HG on proliferation (P<0.001), invasion (P<0.01) and migration (P<0.001) of KYSE30 cells. Conclusions MIR503HG promotes the proliferation, invasion and migration of ESCC cells by regulating hsa-miR-503 pathway and can be used as a new potential target for targeted therapy of ESCC. [ABSTRACT FROM AUTHOR]

Objective To explore the function and mechanism of transcription factor En1 in esophageal squamous cell carcinoma (ESCC). Methods The correlations of En1 with prognosis were analyzed using the overall survival data of 9 397 pan-cancer patients and progression-free survival data of 4 349 pan-cancer patients from The Cancer Genome Atlas (TCGA) database. The En1 expression data in 53 and 155 cases of ESCC and their paired adjacent tissues were from Gene Expression Omnibus (GEO) database and National Genomics Data Center-Genome Sequence Archive (NGDC-GSA)database. Lentivirus was used to generate En1 stable knockout cell lines KYSE180 and KYSE450. The proliferation ability of the cells was detected by cell counting kit 8 and clone formation assay. The migration ability of the cells was detected by Transwell assay. The effect of En1 on the proliferation of ESCC was detected by xenograft experiment in BALB/c-nu/nu mice. Real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) was used to detect the expressions of En1, glioma-associated oncogene family zinc finger 1 (GLI1), glioma-associated oncogene family zinc finger 2 (GLI2) and smoothened (SMO). Results Pan-cancer data from TCGA showed that patients with low En1 expression had longer overall survival and progression-free survival than patients with high En1 expression (P< 0.001). Data from GEO and GSA databases also showed a high expression level of En1 in ESCC tissues compared with paired tissues (P<0.001). Proliferation was inhibited after knockout of En1 in KYSE180 and KYSE450 cells (P<0.001). The colony formation numbers decreased. The colony formation numbers of KYSE180 cells in the shEn1#1 group and the shEn1#2 group were 138.33±23.07 and 127.00±19.70, respectively, significantly lower than that of the shNC group 340.67±12.06 (P<0.001). The colony formation numbers of KYSE450 cells in the shEn1#1 group and the shEn1#2 group were 65.33±2.52 and 9.00±3.00, respectively, significantly lower than that of the shNC group 139.00±13.00 (P<0.001). The migration numbers was inhibited after knockout of En1 [the Transwell numbers of KYSE180 cells in the shEn1#1 group and the shEn1#2 group were 66.67±12.66 and 71.33±11.02, respectively, significantly lower than that of the shNC group 334.67±16.56 (P<0.001). The Transwell numbers of KYSE450 cells in the shEn1#1 group and the shEn1#2 group were 112.33±14.57 and 54.33±5.51, respectively, significantly lower than that of the shNC group 253.33±21.03 (P<0.001)]. Xenograft model showed a slower growth rate of shEn1#1 and shEn1#2 cell lines (P<0.001). The tumor weights of KYSE450 cells in the shEn1#1 group and the shEn1#2 group were (0.046±0.026)g and (0.047±0.025)g, respectively, significantly lower than that of the shNC group (0.130±0.038)g (P<0.001). After knockdown of En1, the relative expression levels of GLI1 in KYSE180 cells of the shEn1#1 group and the shEn1#2 group were 0.326±0.162 and 0.322±0.133, and the relative expression levels of GLI1 in KYSE450 cells of the shEn1#1 and shEn1#2 groups were 0.131±0.006 and 0.352±0.050, respectively, which were all lower than that in the shNC group (P<0.01). After knockdown of En1, overexpression of GLI1 attenuated the inhibitory effect of knockdown of En1 on cell proliferation (P<0.001), colony formation[the colony formation numbers of the shEn1#1-GLI1 group were 151.00±9.54, higher than 102.33±10.02 (P=0.004) of the shEn1#1-vector group] and migration [the migration numbers of the shEn1#1-GLI1 group were 193.67±10.07, higher than 109.33±11.50 (P<0.001) in the shEn1#1-vector group]. In clinical samples of ESCC, major regulatory factors of the Hedgehog pathway were up-regulated and the pathway was activated. Conclusion En1 promotes the proliferation and migration of ESCC cells by regulating the Hedgehog pathway and can be used as a new potential target for targeted therapy of ESCC. [ABSTRACT FROM AUTHOR]

Objective To investigate the expression of long non-coding RNA LOC101927476 (LncRNA LOC101927476) in ovarian cancer and its effect on the biological characteristics of ovarian cancer. Methods Patients with ovarian cancer who underwent surgery in Cancer Hospital of Chinese Academy of Medical Sciences from 2018 to 2019 were selected. The expressions of LOC101927476 in ovarian cancer cells 3AO, OVCA429, TOV21G, A2780, SKOV3, as well as 22 primary tumor tissues and their matched metastatic tumor tissues were detected by real-time quantitative polymerase chain reaction (RT-PCR). Ovarian cancer transcriptome sequencing data from the TCGA database was used to verify the expressions of LOC101927476 and GATA4. 3AO and OVCA429 cells were infected with lentivirus plasmid containing OE-LOC101927476 and single guide RNA (sg-RNA) targeting LOC101927476, respectively. The effects of LOC101927476 on migration and invasion were detected by Transwell and wound healing assay. The effect of LOC101927476 on cell proliferation was detected by cell counting kit-8 (CCK-8) assay. Results RT-PCR assay showed that 20 out of 22 patients had significantly lower expression of LOC101927476 in their metastatic tumors compared with primary tumors. Transwell assay showed that overexpression of LOC101927476 significantly inhibited the invasion and migration capacities of 3AO cells. The numbers of invading and migrating 3AO cells infected with OE-LOC101927476 lentivirus were (357±63) and (699±65), respectively, lower than (661±95) and (1 024±76) in OE-EV group (P<0.050). In contrast, the numbers of invading and migrating OVCA429 cells with LOC101927476 knockdown were (512±72) and (472±40), respectively, higher than (309±13) and (363±27) in sg-Control group (P<0.050). Wound healing assay results showed that after 48 hours, the percentage of scratch healing of 3AO cells in OE-LOC101927476 group was (10.86±0.63)%, significantly lower than (57.38±4.42)% of OE-EV group (P=0.009). After 24 hours, the percentage of scratch healing of OCVA429 cells in sg-LOC101927476 group was (59.98±1.34)%, significantly higher than (23.15±2.03)% of sg-Control group (P=0.004). CCK-8 assays showed that the OD value of 3AO cells in OE-LOC101927476 group was (2.07±0.08), significantly lower than (2.29±0.04) of OE-EV group (P=0.009). The OD value of OVCA429 cells in sg-LOC101927476 group was (2.13±0.03), significantly higher than (1.93±0.03) of sg-Control group (P=0.001). The relative expression of GATA4 in OE-LOC101927476 group was (1.86±0.25), significantly higher than 1.00 of OE-EV group (P=0.001). In patients with high expression of LncRNA LOC101927476, the expression level of GATA4 was (2.93±0.35), which was higher than (0.29±0.06) of LOC101927476 low expression group (P=0.001). Conclusion LncRNA LOC101927476 can inhibit the invasion, migration and proliferation of ovarian cancer cells. [ABSTRACT FROM AUTHOR]

Objective To clarify the function and molecular mechanisms of serpin family E member 2 (SERPINE2) in cellular migration and invasion of esophageal squamous cell carcinoma (ESCC). Methods The expression of SERPINE2 in ESCC was analyzed by using online databases TCGA (http: //gepia.cancer-pku.cn/detail.php and http: //ualcan.path.uab. edu/index.html). The expressions of SERPINE2 mRNA in normal human esophageal epithelial cell line NE2, human ESCC cell lines KYSE30 and KYSE150 were detected by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). SERPINE2-konckdown or SERPINE2-overexpressed plasmid was transfected into KYSE30 cells, and the efficiencies of the knockdown and overexpression system were tested by qRT-PCR. The relationships of SERPINE2 and ESCC migration and invasion were determined by migration and invasion assays in vitro. The associations between SERPINE2 expression and β-catenin as well as its target genes including c-Myc, cyclin D1 and CD44 were analyzed by immunofluorescence, qRT-PCR and western blot, respectively. Results The expressions of SERPINE2 were significantly upregulated in both esophageal cancer (ESCA) and ESCC tissues compared to normal tissues by analyzing 182 and 95 cases, respectively (P<0.01). SERPINE2 is highly expressed in both KYSE30 and KYSE150 cells (P<0.05). The number of migrating and invading cells in control group were (212.66±24.11)/field and (136.00±14.42)/field, while were (88.33±9.71)/field and (77.00±9.53)/field in SERPINE2-knockdown 1 group, and (66.00±8.00)/field and (45.66±3.78)/field in SERPINE2-knockdown 2 group, respectively, and the differences were dramatically significant compared with the control group (P<0.01). The number of migrating and invading cells in control group were (250.00±30.00)/field and (203.33±15.27)/field, while were (383.33±35.11)/field and (246.66±25.16)/field in SERPINE2-overpressed group, and the differences were strikingly significant compared with the control group (P<0.01). The protein expression of β-catenin was upregulated while phosphorylated β-catenin protein expression was downregulated in SERPINE2-overexpressed KYSE30 cells when compared to control cells.The transcription activity of β-catenin was significantly upregulated and the mRNA expressions of its target genes including c-Myc, cyclin D1 and CD44 were all increased. After treated with 25 μM iCRT14, the number of migrated cells in the control and SERPINE2-overpressed groups were (200.00±36.05)/field and (258.33±22.54)/field, and the number of invaded cells were (160.00±17.32)/field and (188.33±25.65)/field, respectively, the differences were dramatically significant compared with the group without iCRT14 treatment (P<0.01). Conclusion SERPINE2 is significantly upregulated in ESCC cells and can promote cellular migration and invasion by activating β-catenin, which may provide a potential therapeutic target for patients with ESCC. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of UChL5 on proliferation and apoptosis of breast cancer cells. Methods SW527 cells were infected with lentiviral vector carrying short hairpin RNA to delete the expression of UChL5. 3-(4, 5-dimethylithiazol-2-yl) -5-(3-carboxymethoxyphenyl) -2-(4-sulfophenyl) -2h-tetrazolium (MTS) assay was used to examine cell proliferation, and subcutaneous transplantation experiments were performed to detect tumor growth. Cell apeepteesis was deteeteel using Annexin V/ Propidium iodide (PI) double staining. The cirrelation between UChL5 expression and the expressions of proliferation and apoptosis associated genes was analyzed using TCGA breast invasive carcinoma data set. The ralationship between UChL5 expressions and breast cancer patients' survival was analyzeel using Kaplan-Meier Plotter online tool. Results After knockdown of UChL5, A values of SW527 cells on day 2 and day 4 were 0.822±0.017 and 1.045±0.023, respectively, which were significantly lower than 0.976±0.016 and 1.284±0.025 of control cells on day 2 and day 4 (P<0.001). In vivo xenografted mouse model, the volume in UChL5-suppressed group was (166.90±75.05) mm3, significantly smaller than (329.80±35.84) mm3 in control group (P = 0.029). Flow cytometry analysis showed the apoptotic rate erf SW527 cells was (8.60±1.13)% after knockdown of UChL5, significantly higher than (2.95±0.07)% of control group (P = 0.020). TCGA database analysis showed that the expression of UCHL5 was positively correlated with the' expressions of genes related to cell proliferation, in paraded with the increased expression of UChL5, the expression of the pro-apoptosis associated genes was decreased. Kaplan-Meier Plotter analysis demonstrated that the overall survival and relapse-free survival of breast cancer patients with high expression of UCI1L5 were mueh shorter (all P<0.001). Conclusions Down-regulation of UChL5 inhibits the proliferation and tumor formation and promotes apoptosis of SW527 cells. high expression of UChL5 may predict poor prognosis of breast cancer patients. [ABSTRACT FROM AUTHOR]

Objective To explore the expression of S100A14 in breast cancer tissue, and the EGF and S100A14 feedback regulatory mechanism. Methods S100A14 mRNA level in 52 cases of of breast cancer and adjacent normal tissue was detected by quantitative real-time PCR. S100A14 protein in 21 cases of breast cancer and adjacent normal tissue was detected by Western blot. S100A14 mRNA after EGF treatment was detected by RT-PCR and real-time PCR. The levels of S100A14, p-ERK and t-ERK were detected by Western blot. Knocking down S100A14 expression was performed by siRNA technology. Results The levels of S100A14 mRNA and protein were significantly increased in breast cancer tissues (P<0.05 for both). The high expression of S100A14 was related with the recurrence of breast cancer patients (P= 0.038). S100A14 mRNA level was significantly up-regulated in the MDA-MB-453 cells (1.50±0.11) and MCF-7 cells (1.40±0.03) after 1 ng/mL EGF treatment, and 1.66±0.08 and 1.71±0.17 in the MDA-MB-453 cells after 10 ng/mL EGF treatment, significantly higher than that of the control group (1.00±0.09 and 1.00±0.03) (P<0.05 for both). In the TD47 cells, the S100A14 mRNA levels in the control, 1 ng/ml EGF and 10 ng/ml EGF + U0126 treatment groups were 1.00±0.04, 1.56±0.04 and 1.00±0.10, respectively (P<0.05). Conclusions The expression of S100A14 mRNA and protein is promoted by EGF through p-ERK signaling pathway in breast cancer cells. There may be a feedback loop between EGF and S100A14. [ABSTRACT FROM AUTHOR]

Ｏｂｊｅｃｔｉｖｅ 　Ｔｏ ｉｎｖｅｓｔｉｇａｔｅ ｔｈｅ ｃｈａｎｇｅｓ ｏｆ ＩＤ１ ｅｘｐｒｅｓｓｉｏｎ ｉｎ ｔｕｍｏｒ ｃｅｌｌｓ ｔｒｅａｔｅｄ ｗｉｔｈ ｅｔｏｐｏｓｉｄｅ， ｃｉｓｐｌａｔｉｎ ａｎｄ ｕｌｔｒａｖｉｏｌｅｔ （ＵＶ） ｉｒｒａｄｉａｔｉｏｎ， ａｎｄ ｅｘｐｌｏｒｅ ｔｈｅ ｅｆｆｅｃｔ ｏｆ ＩＤ１ ｏｎ ｃｈｅｍｏｔｈｅｒａｐｅｕｔｉｃ ｄｒｕｇ⁃ ａｎｄ ＵＶ⁃ｉｎｄｕｃｅｄ ａｐｏｐｔｏｓｉｓ． Ｍｅｔｈｏｄｓ 　Ｉｎ ｔｈｅ ｐｒｅｓｅｎｔ ｓｔｕｄｙ， ｕｐｏｎ ｏｎｓｅｔ ｏｆ ａｐｏｐｔｏｓｉｓ ｉｎｄｕｃｅｄ ｂｙ ｖａｒｉｏｕｓ ｋｉｎｄｓ ｏｆ ｉｎｄｕｃｅｒｓ ｓｕｃｈ ａｓ ｅｔｏｐｏｓｉｄｅ， ｃｉｓｐｌａｔｉｎ ａｎｄ ＵＶ ｉｒｒａｄｉａｔｉｏｎ， ｔｈｅ ｅｘｐｒｅｓｓｉｏｎ ｌｅｖｅｌ ｏｆ ＩＤ１ ｗａｓ ｄｅｔｅｃｔｅｄ ｂｙ Ｗｅｓｔｅｒｎ ｂｌｏｔ ａｎｄ ｒｅａｌ⁃ｔｉｍｅ ＰＣＲ． Ｗｅ ａｌｓｏ ａｎａｌｙｚｅｄ ｔｈｅ ｈａｌｆ⁃ｌｉｆｅ ｏｆ ＩＤ１ ｐｒｏｔｅｉｎ ａｎｄ ｓｔａｂｉｌｉｔｙ ｏｆ ＩＤ１ ｍＲＮＡ ｒｅｓｐｅｃｔｉｖｅｌｙ ｂｙ ｃｙｃｌｏｈｅｘｉｍｉｄｅ ｉｎｈｉｂｉｔｉｏｎ ｔｅｓｔ ａｎｄ ＲＴ⁃ＰＣＲ． Ａｎｎｅｘｉｎ⁃Ｖ ａｓｓａｙ ｗａｓ ｃａｒｒｉｅｄ ｏｕｔ ｔｏ ｅｖａｌｕａｔｅ ｔｈｅ ｃｏｎｔｒｉｂｕｔｉｏｎ ｏｆ ＩＤ１ ｐｒｏｔｅｉｎ ｔｏ ｃｈｅｍｏｔｈｅｒａｐｅｕｔｉｃ ｄｒｕｇ⁃ ａｎｄ ＵＶ⁃ｉｎｄｕｃｅｄ ａｐｏｐｔｏｓｉｓ． Ｒｅｓｕｌｔｓ　ＩＤ１ ｅｘｐｒｅｓｓｉｏｎ ｐｒｅｓｅｎｔｅｄ ａ ｐｒｏｆｏｕｎｄ ｄｏｗｎ⁃ｒｅｇｕｌａｔｉｏｎ ｉｎ ｔｈｅ ＨＣＴ１１６ ｃｅｌｌｓ ｔｒｅａｔｅｄ ｗｉｔｈ ｅｔｏｐｏｓｉｄｅ， ｃｉｓｐｌａｔｉｎ ａｎｄ ＵＶ ｉｒｒａｄｉａｔｉｏｎ（Ｐ＜０．０５ ｆｏｒ ａｌｌ）． Ｔｈｅ ａｐｏｐｔｏｓｉｓ ｉｎ ｔｈｅ ＵＶ ｉｒｒａｄｉａｔｉｏｎ ｇｒｏｕｐ， ｃｉｓｐｌａｔｉｎ ｇｒｏｕｐ， ｅｔｏｐｏｓｉｄｅ ｇｒｏｕｐ ｗａｓ （５８．７０±１．５５）％， （３５．８０±０．９２）％ ａｎｄ （２１．００±０．７２）％， ｒｅｓｐｅｃｔｉｖｅｌｙ， ｓｉｇｎｉｆｉｃａｎｔｌｙ ｈｉｇｈｅｒ ｔｈａｎ ｔｈａｔ ｏｆ ｔｈｅ ｃｏｎｔｒｏｌ ｇｒｏｕｐ（１．１０±０．０７）％， （１．２０±０．１３）％ ａｎｄ （３．５０±０．２３）％ （Ｐ＜０．０５ ｆｏｒ ａｌｌ）． Ｕｐｏｎ ｅｔｏｐｏｓｉｄｅ ｔｒｅａｔｍｅｎｔ， ＩＤ１ ｅｘｐｒｅｓｓｉｏｎ ｌｅｖｅｌ ｗａｓ ｄｅｃｒｅａｓｅｄ ｖｉａ ｉｎｄｕｃｔｉｏｎ ｏｆ ｍＲＮＡ ｉｎｓｔａｂｉｌｉｔｙ， ｂｕｔ ｎｏｔ ｔｈｅ ｐｒｏｔｅｉｎ ｄｅｇｒａｄａｔｉｏｎ ｃｈａｎｇｅｓ． Ａｄｄｉｔｉｏｎａｌｌｙ， ｅｃｔｏｐｉｃ ｅｘｐｒｅｓｓｉｏｎ ｏｆ ＩＤ１ ｉｎ ｔｈｅ ＨＣＴ１１６ ｃｅｌｌｓ ａｌｌｅｖｉａｔｅｄ ｅｔｏｐｏｓｉｄｅ⁃， ｃｉｓｐｌａｔｉｎ⁃ ａｎｄ ＵＶ⁃ｉｎｄｕｃｅｄ ａｐｏｐｔｏｓｉｓ． Ｔｈｅ ｒｅｓｕｌｔｓ ｏｆ ｆｌｏｗ ｅｙｔｏｍｅｔｒｙ ｒｅｖｅａｌｅｄ ｔｈａｔ ｔｈｅ ｐｅｒｃｅｎｔａｇｅ ｏｆ ａｐｏｐｔｏｔｉｃ ｃｅｌｌｓ ｉｎ ｔｈｅ ＩＤ１ ｇｒｏｕｐ ｕｎｄｅｒ ｔｈｅ ｔｒｅａｔｍｅｎｔ ｏｆ ｅｔｏｐｏｓｉｄｅ， ｃｉｓｐｌａｔｉｎ ａｎｄ ＵＶ ｉｒｒａｄｉａｔｉｏｎ ｗａｓ （２３．８０±０．８２）％， （１７．８０±１．３４）％ ａｎｄ （１３．４０±０．５３）％， ｒｅｓｐｅｃｔｉｖｅｌｙ， ｓｉｇｎｉｆｉｃａｎｔｌｙ ｌｏｗｅｒ ｔｈａｎ ｔｈａｔ ｉｎ ｔｈｅ ｅｍｐｔｙ ｖｅｃｔｏｒ ｇｒｏｕｐ （４１．１０± １．６１）％， （３０．４０± ２．６７）％ ａｎｄ （２２．５０± ３．４７）％ （Ｐ ＜ ０．０５ ｆｏｒ ａｌｌ）． Ｃｏｎｃｌｕｓｉｏｎｓ 　Ｔｈｅｓｅ ｏｂｓｅｒｖａｔｉｏｎｓ ｉｎｄｉｃａｔｅ ｔｈａｔ ｔｈｅ ｔｒｅａｔｍｅｎｔ ｗｉｔｈ ｅｔｏｐｏｓｉｄｅ ｒｅｄｕｃｅｓ ｔｈｅ ａｍｏｕｎｔ ｏｆ ＩＤ１ ｂｙ ｉｎｄｕｃｔｉｏｎ ｏｆ ｍＲＮＡ ｉｎｓｔａｂｉｌｉｔｙ， ａｎｄ ｅｘｏｇｅｎｏｕｓｌｙ ｉｎｔｒｏｄｕｃｅｄ ＩＤ１ ｐｒｏｔｅｃｔｓ ｃｅｌｌｓ ａｇａｉｎｓｔ ｅｔｏｐｏｓｉｄｅ⁃， ｃｉｓｐｌａｔｉｎ⁃ ａｎｄ ＵＶ ｉｒｒａｄｉａｔｉｏｎ⁃ｉｎｄｕｃｅｄ ａｐｏｐｔｏｓｉｓ． Ｉｎｈｉｂｉｔｉｏｎ ｏｆ ｔｈｅ ＩＤ１ ｂｉｏａｃｔｉｖｉｔｙ ｍａｙ ｂｅｃｏｍｅ ａ ｎｅｗ ｓｔｒａｔｅｇｙ ｉｎ ｃａｎｃｅｒ ｔｒｅａｔｍｅｎｔ． [ABSTRACT FROM AUTHOR]