Expression and clinical significance of AKR1B10 in hepatocellular carcinoma by TCGA database analysis

doi:10.3877/cma.j.issn.1674-3946.2021.04.008

Abstract

Abstract:

Objective

To investigate the expression and clinical value of AKR1B10 in hepatocellular carcinoma, and to explore the role of AKR1B10 in the development of hepatocellular carcinoma.

Methods

The hepatocellular carcinoma dataset was downloaded from the Cancer Gene Map (TCGA) database to obtain the AKR1B10 gene expression profile and clinical information on October 15, 2019. Thecorrelation between the expression of AKR1B10 in 424 samples and the prognosis and clinicopathological features of hepatocellular carcinoma were analyzed. Gene-enrichment analysis (GSEA) were used to predict the regulatory pathway of AKR1B10 in hepatocellular carcinoma. Statistical analysis was performed by using SPSS22.0 software Independent t test was used to detect the difference of expression between liver cancer tissues and adjacent tissues. The correlation of clinicopathological parameters between two groups was analyzed by chi-square test. Cox regression model was used for univariate and multivariate analysis. A P value of<0.05 was considered as statistically significant difference.

Results

AKR1B10 was highly expressed in hepatocellular carcinoma, and the overall survival rate of patients with high expression of AKR1B10 was significantly lower than that of patients with low expression of AKR1B10 (P=0.006). Multivariate analysis further indicated that AKR1B10 expression was an independent risk factor affecting the prognosis of HCC (P=0.003). AKR1B10 expression were enriched into toll-like receptor signaling pathway, nod-like receptor signaling pathway, aminoacyl tRNA biosynthetic, glutathione metabolism.

Conclusion

High expression of AKR1B10 mRNA in liver cancer tissues is a risk factor for poor prognosis. Rt-PCR could be used to rapidly detect the expression of AKR1B10 mRNA in liver cancer tissues to evaluate the prognosis of patients, which is a new indicator for predicting the prognosis of patients with hepatocellular carcinoma.

Key words: Carcinoma, hepatocellular, Aldo-keto reductase family1, member B10, Gene expression, The cancer genome atlas, Clinical significance

Rongqiang Liu, Shiyang Zheng, Tianxing Dai, Minbing Deng, Guozhen Lin, Chaorong Zhou, Guoying Wang. Expression and clinical significance of AKR1B10 in hepatocellular carcinoma by TCGA database analysis[J]. Chinese Journal of Operative Procedures of General Surgery(Electronic Edition), 2021, 15(04): 380-383.

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References 22

[1]	Forner A, Reig M, Bruix J. Hepatocellular carcinoma [J]. Lancet (London, England), 2018, 391(10127): 1301-1314.
[2]	Zheng W, Jiang F, Shan J, et al. Levels of serum IgG subclasses in patients with liver disease: A retrospective study[J]. Exp Ther Med, 2020, 21(1): 45-54.
[3]	Zeng J, Zeng J, Wu Q, et al. Novel inflammation-based prognostic nomograms for individualized prediction in hepatocellular carcinoma after radical resection[J]. Ann Transl Med, 2020, 8(17): 1061.
[4]	Kang S-O, Kwak M-K. Alcohol dehydrogenase 1 and NAD(H)-linked methylglyoxal oxidoreductase reciprocally regulate glutathione-dependent enzyme activities in Candida albicans[J]. J Microbiol, 2021, 59(1): 76-91.
[5]	Fang C-Y, Lin Y-H, Chen C-L. Overexpression of akr1b10 predicts tumor recurrence and short survival in oral squamous cell carcinoma patients[J]. J Oral Pathol Med , 2019, 48(4): 712-719.
[6]	Hung J-J, Yeh Y-C, Hsu W-H. Prognostic significance of akr1b10 in patients with resected lung adenocarcinoma[J]. Thorac Cancer, 2018, 9(11): 1492-1499.
[7]	Ahmed SMU, Jiang ZN, Zheng ZH, et al. AKR1B10 expression predicts response of gastric cancer to neoadjuvant chemotherapy[J]. Oncol Lett, 2019, 17(1): 773-780.
[8]	Ha SY, Song DH, Lee JJ, et al. High expression of aldo-keto reductase 1b10 is an independent predictor of favorable prognosis in patients with hepatocellular carcinoma[J]. Gut Liver, 2014, 8(6): 648-654.
[9]	Wang Y-Y, Qi L-N, Zhong J-H, et al. High expression of AKR1B10 predicts low risk of early tumor recurrence in patients with hepatitis B virus-related hepatocellular carcinoma[J]. Sci Rep, 2017, 7: 42199.
[10]	Jin J, Liao W, Yao W, et al. Aldo-keto reductase family 1 member b 10 mediates liver cancer cell proliferation through sphingosine-1-phosphate[J]. Sci Rep, 2016, 6: 22746.
[11]	Wang J, Zhou Y, Fei X, et al. Biostatistics mining associated method identifies AKR1B10 enhancing hepatocellular carcinoma cell growth and degenerated by miR-383-5p[J]. Sci Rep, 2018, 8(1): 11094.
[12]	Elebo N, Fru P, Omoshoro-Jones J, et al. Role of different immune cells and metabolic pathways in modulating the immune response in pancreatic cancer (Review)[J]. Mol Med Rep, 2020, 22(6): 4981-4991.
[13]	Khayami R, Hashemi SR, Kerachian MA. Role of aldo-keto reductase family 1 member B1 (AKR1B1) in the cancer process and its therapeutic potential[J]. J Cell Mol Med, 2020, 24(16): 8890-8902.
[14]	Taskoparan B, Seza EG, Demirkol S, et al. Opposing roles of the aldo-keto reductases AKR1B1 and AKR1B10 in colorectal cancer[J]. Cell Oncol (Dordr), 2017, 40(6): 563-578.
[15]	Yao Y, Wang X, Zhou D, et al. Loss of AKR1B10 promotes colorectal cancer cells proliferation and migration via regulating FGF1-dependent pathway[J]. Aging (Albany NY), 2020, 12(13): 13059-13075.
[16]	Li J, Guo Y, Duan L, et al. AKR1B10 promotes breast cancer cell migration and invasion via activation of ERK signaling[J]. Oncotarget, 2017, 8(20): 33694-33703.
[17]	Zu X, Yan R, Pan J, et al. Aldo-keto reductase 1B10 protects human colon cells from DNA damage induced by electrophilic carbonyl compounds[J]. Mol Carcinog, 2017, 56(1): 118-129.
[18]	Liu F-Y, Fang B-Q, Sun L-M, et al. The Role of the NOD1/Rip2 Signaling Pathway in Myocardial Remodeling in Spontaneously Hypertensive Rats[J]. Med Sci Monit, 2020, 26: e924748.
[19]	Udden SMN, Peng L, Gan J-L, et al. Nod2 suppresses colorectal tumorigenesis via downregulation of the tlr pathways[J]. Cell Rep, 201, 19(13): 2756-2770.
[20]	Ayala-Cuellar AP, Cho J, Choi K-C. Toll-like receptors: A pathway alluding to cancer control[J]. J Cell Physiol, 2019, 234(12): 21707-21715.
[21]	Hyeon DY, Kim JH, Ahn TJ, et al. Evolution of the multi-tRNA synthetase complex and its role in cancer[J]. J Biol Chem, 2019, 294(14): 5340-5351.
[22]	Xu Y, Zheng X, Bai X, et al. Simultaneous integrated boost intensity-modulated radiotherapy for locally advanced non-small cell lung cancer in chinese population: A retrospective study[J]. Oncotarget, 2017, 8(30): 49084-49092.

变量	单因素分析		多因素分析
变量	HR(95%CI)	P值	HR(95%CI)	P值
年龄	1.01(0.99～1.02)	0.59	1(0.98～1.02)	0.7
性别	0.78(0.49～1.25)	0.3	0.77(0.44～1.32)	0.337
病理分级	1.02(0.75～1.39)	0.91	1.08(0.76～1.52)	0.678
病理分期	1.86(1.46～2.39)	<0.01	1.41(0.54～3.69)	0.48
T分期	1.8(1.43～2.27)	<0.01	1.38(0.6～3.22)	0.45
M分期	3.85(1.21～12.28)	0.02	0.81(0.21～3.13)	0.759
N分期	2.02(0.49～8.28)	0.33	1.77(0.23～13.32)	0.58
AKR1B10	1.09(1.01～1.17)	0.02	1.13(1.04～1.22)	0.003

变量	单因素分析		多因素分析
变量	HR(95%CI)	P值	HR(95%CI)	P值
年龄	1.01(0.99～1.02)	0.59	1(0.98～1.02)	0.7
性别	0.78(0.49～1.25)	0.3	0.77(0.44～1.32)	0.337
病理分级	1.02(0.75～1.39)	0.91	1.08(0.76～1.52)	0.678
病理分期	1.86(1.46～2.39)	<0.01	1.41(0.54～3.69)	0.48
T分期	1.8(1.43～2.27)	<0.01	1.38(0.6～3.22)	0.45
M分期	3.85(1.21～12.28)	0.02	0.81(0.21～3.13)	0.759
N分期	2.02(0.49～8.28)	0.33	1.77(0.23～13.32)	0.58
AKR1B10	1.09(1.01～1.17)	0.02	1.13(1.04～1.22)	0.003

变量	N	OR	P
分期(III-IV vs. I-II)	353	0.58(0.36～0.95)	0.03
转移(M1 vs. M0)	276	3.05(0.38～62)	0.34
T分期(T3-4 vs. T1-2)	374	0.6(0.38～0.98)	0.04
N分期(N2-3 vs. N0-1)	261	0.33(0.02～2.6)	0.34
分级(g3-4 vs. G1-2)	372	1.05(0.69～1.61)	0.83

变量	N	OR	P
分期(III-IV vs. I-II)	353	0.58(0.36～0.95)	0.03
转移(M1 vs. M0)	276	3.05(0.38～62)	0.34
T分期(T3-4 vs. T1-2)	374	0.6(0.38～0.98)	0.04
N分期(N2-3 vs. N0-1)	261	0.33(0.02～2.6)	0.34
分级(g3-4 vs. G1-2)	372	1.05(0.69～1.61)	0.83

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