Expression and potential role of Kir4.1 in malignant gliomas: database combined with document analysis

doi:10.3877/cma.j.issn.2095-9141.2021.04.008

Abstract

Abstract:

Objective

To explore the expression of inward rectifier potassium channel Kir4.1 in malignant gliomas and its correlation and correlation mechanism with epilepsy, edema and other symptoms of gliomas through database and document analysis.

Methods

Oncomine database was used to analyze the expression of glioblastoma compared with normal brain tissue in TCGA data set. Specimens and pathological information of patients with different clinical grades of glioma were collected to analyze the expression of Kir4.1 in different grades of glioma. Kir4.1 mutations in gliomas were analyzed by cbioportal database.

Results

The results of oncomine database showed great differences due to the differences of sample size. RT-PCR and immunohistochemistry showed that the expression of Kir4.1 in high-grade glioma was less than in low-grade glioma, but the expression of Kir4.1 in low-grade glioma was higher than in normal brain tissues, and the difference was statistically significant (P<0.05). The cbioportal database showed that the mutation probability of Kir4.1 was extremely low in glioblastoma, and the difference between partial genome alteration and the number of mutations was statistically significant (P<0.05). MSH2, ERRFI1, CTNNB1, SEPRINE1, FOXM1, RAD50 and other genes were highly expressed in the altered group, while INPP4B, XBP1, AXL and other genes were highly expressed in the non-altered group.

Conclusion

The expression of Kir4.1 is different in different grades of glioma. High grade glioma has lower expression of Kir4.1, and the expression of Kir4.1 may be related to epilepsy, edema and other clinical symptoms in patients with high grade glioma, which provides a new idea for exploring the potential mechanism of Kir4.1 in glioblastoma in the future.

Key words: Glioblastoma, Inward rectifier potassium channel Kir4.1, Epilepsy, Edema, Proliferation

Chan Zhang, Qiang Xue, Ruifeng Tian, Xiaoyan Chen. Expression and potential role of Kir4.1 in malignant gliomas: database combined with document analysis[J]. Chinese Journal of Neurotraumatic Surgery(Electronic Edition), 2021, 07(04): 224-234.

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Figures/Tables 9

References 20

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序号	ATRX	BRAF	CD34	EGFR	EMA	GFAP	Ki67	NF	MGMT	Neun	Olig-2	P53	S-100	Syn	Vim	1P	19q	IDH1	IDH	级别
P1			-	-	-	+	5%	+	-		+	-	+	-	-			R132H+		Ⅱ
P2	±					+	5%		-		+	±	+	-	-	缺失	缺失	R133H突变		Ⅱ
P3			-	+	-	+	12%		-		+	-		+	-			R132H+		Ⅱ
P4					-	+	20-30%	+				-	+		+					Ⅱ
P5	+	VE1(-)	血管+		-	星形象胞+	（+，局部约20%)	+		残余神经元+	+	（+，约10%)	+	+		缺失	缺失			Ⅱ
P6						+							+	灶+						Ⅱ
P7						+	6%						+	+						Ⅱ
P8	灶+	VE1(-)	血管+		-	+	2%	+	-	+	+		+	-	-			R132H(-)		Ⅱ
P9	+	VE1(-)	-	+	-	+	8%	+	（+，约5%）		+	散在+	+	-	-	缺失	缺失	R132H突变		Ⅱ
P10	+	VE1(-)	-	+	-	+	6%	+	+		+	-	+	灶+	-	缺失	缺失	R132H(+)	突变	Ⅱ
P11	+	VE1(-)	-	+	-	+	2%	+	（+，约10%）	节细胞+	+	灶+	+	+	-	缺失	缺失	R132H(+)	突变	Ⅱ
P12	+	VE1(-)	血管+	+	-	+	（+，局部约5%)		（+，约15%）		+	-	+	-	-	缺失	缺失	R132H突变	突变	Ⅱ
P13	+	VE1(-)	-		-	+	（+，约4%）	-	（+，约10%）		+	-	+	-	-	缺失	缺失	R132H突变	突变	Ⅱ
P14	局部+	VE1(-)	-	+	-	+	15%				+	散在+	+	部分+	-	缺失	缺失	R132H突变	突变	Ⅱ
P15	+	V600E(-)	-	+	-	+	（+，局部约15%)	-	-		+	少数+	+	+	-	缺失	缺失	+	突变	Ⅱ
P16	+	V600E(-)	-	+	-	+	（+，约15%）	-	部分-，检测到基因启动子区甲基化水平为43%+		+	-	+	+	-	缺失	缺失	+	突变	Ⅱ
P17			-			+	2%		+	-	+		+	+	+					Ⅱ
P18	部分+		血管+		-	+	（+，局部约6%)	+	-		+	-	+	+	+	缺失	缺失	R132H(-)	突变	Ⅱ
P19	+		-		灶+	+	12%	小灶弱+	-		+		+	小灶+	-	缺失	缺失	R132H(+)	突变	Ⅱ
P20						+	（+，局部约8%)		-											Ⅱ

序号	ATRX	BRAF	CD34	EGFR	EMA	GFAP	Ki67	NF	MGMT	Neun	Olig-2	P53	S-100	Syn	Vim	1P	19q	IDH1	IDH	级别
P1			-	-	-	+	5%	+	-		+	-	+	-	-			R132H+		Ⅱ
P2	±					+	5%		-		+	±	+	-	-	缺失	缺失	R133H突变		Ⅱ
P3			-	+	-	+	12%		-		+	-		+	-			R132H+		Ⅱ
P4					-	+	20-30%	+				-	+		+					Ⅱ
P5	+	VE1(-)	血管+		-	星形象胞+	（+，局部约20%)	+		残余神经元+	+	（+，约10%)	+	+		缺失	缺失			Ⅱ
P6						+							+	灶+						Ⅱ
P7						+	6%						+	+						Ⅱ
P8	灶+	VE1(-)	血管+		-	+	2%	+	-	+	+		+	-	-			R132H(-)		Ⅱ
P9	+	VE1(-)	-	+	-	+	8%	+	（+，约5%）		+	散在+	+	-	-	缺失	缺失	R132H突变		Ⅱ
P10	+	VE1(-)	-	+	-	+	6%	+	+		+	-	+	灶+	-	缺失	缺失	R132H(+)	突变	Ⅱ
P11	+	VE1(-)	-	+	-	+	2%	+	（+，约10%）	节细胞+	+	灶+	+	+	-	缺失	缺失	R132H(+)	突变	Ⅱ
P12	+	VE1(-)	血管+	+	-	+	（+，局部约5%)		（+，约15%）		+	-	+	-	-	缺失	缺失	R132H突变	突变	Ⅱ
P13	+	VE1(-)	-		-	+	（+，约4%）	-	（+，约10%）		+	-	+	-	-	缺失	缺失	R132H突变	突变	Ⅱ
P14	局部+	VE1(-)	-	+	-	+	15%				+	散在+	+	部分+	-	缺失	缺失	R132H突变	突变	Ⅱ
P15	+	V600E(-)	-	+	-	+	（+，局部约15%)	-	-		+	少数+	+	+	-	缺失	缺失	+	突变	Ⅱ
P16	+	V600E(-)	-	+	-	+	（+，约15%）	-	部分-，检测到基因启动子区甲基化水平为43%+		+	-	+	+	-	缺失	缺失	+	突变	Ⅱ
P17			-			+	2%		+	-	+		+	+	+					Ⅱ
P18	部分+		血管+		-	+	（+，局部约6%)	+	-		+	-	+	+	+	缺失	缺失	R132H(-)	突变	Ⅱ
P19	+		-		灶+	+	12%	小灶弱+	-		+		+	小灶+	-	缺失	缺失	R132H(+)	突变	Ⅱ
P20						+	（+，局部约8%)		-											Ⅱ

序号	ATRX	BRAF	CD34	EGFR	EMA	GFAP	Ki67	NF	MGMT	Olig-2	P53	S-100	Syn	Vim	19q	IDH1	IDH	级别
P1	+		血管+	小灶+	-	-	15%	-	-	-	-	灶+	-	弱+			野生型	Ⅳ
P2	+	VE1(-)	血管+	+	-	+	15%	-	-	+	异常膜+	+	弱+	+	缺失		野生型	Ⅳ
P3	部分+		-		-	+	局部60%	+	+	+	部分+	+	灶+	0		R132H(-)	野生型	Ⅳ
P4	+	VE1(-)	血管+	+	-	+	15%	-	-	+	异常膜+	+	弱+	+	缺失		野生型	Ⅳ
P5	-	VE1(-)	-	+	-	+	40%	-	±	(+/-)	(-/+)	+	-	(+/-)			H3K27M突变型	Ⅳ
P6	+		-			+	80%	-	-	+	+	+	弱+	-			野生型	Ⅳ
P7	-		-	+	-	+	30%	-	-	+	散在+	+	-	-			野生型	Ⅳ
P8	+		-			+	80%		±	+	+	+	-	散在+		R132H(-)	野生型	Ⅳ
P9	+	VE1(-)	血管+	-	-	+	45%		<5%	+	野生型	+	+	+			野生型	Ⅳ
P10	+	VE1(-)	-	+	-	+	40%	-	+,约40%	+	+	+	-	-		R132H(-)	野生型	Ⅳ
P11	-	VE1(-)	-	+	-	局灶+	70%	-	±	-	弥漫强+	局灶+	-	+			胶质母细胞瘤	Ⅳ
P12	+		-		-	灶+	60%	-	-	+	+,突变型表达	+	小灶+	-			野生型	Ⅳ
P13		VE1(-)	显示血管增生	+	-	+	60%	-	+,约5%	+	弥漫+，突变型表达	+	-	-			IDH1/2野生型	Ⅳ
P14	+		+	+	局部+	+	+，局部约35%	-	-	局部+	-	+	-	+			野生型	Ⅳ
P15	+		-		-	+	60%	-	-	+	弥漫强+	+	-	+			野生型	Ⅳ
P16	+	VE1(-)	-	+	-	+	+,15%	-	-	+	+	+	-	+		R132H(-)	野生型	Ⅳ
P17	-		-		±	+	40%	+	+,15%	+	+	+	-	+			IDH1突变型	Ⅳ
P18	+	VE1(-)	-	-	-	+	30%	+	-	+	+	+	-	+			野生型	Ⅳ
P19	-	VE1(-)	-	-	-	+	30%	-	-	+	散在+	+	局部+	+			野生型	Ⅳ
P20	+	VE1(-)	-	+	-	-	50%	-	-	+	灶+	+	-	+		R132H(-)	野生型	Ⅳ

序号	ATRX	BRAF	CD34	EGFR	EMA	GFAP	Ki67	NF	MGMT	Olig-2	P53	S-100	Syn	Vim	19q	IDH1	IDH	级别
P1	+		血管+	小灶+	-	-	15%	-	-	-	-	灶+	-	弱+			野生型	Ⅳ
P2	+	VE1(-)	血管+	+	-	+	15%	-	-	+	异常膜+	+	弱+	+	缺失		野生型	Ⅳ
P3	部分+		-		-	+	局部60%	+	+	+	部分+	+	灶+	0		R132H(-)	野生型	Ⅳ
P4	+	VE1(-)	血管+	+	-	+	15%	-	-	+	异常膜+	+	弱+	+	缺失		野生型	Ⅳ
P5	-	VE1(-)	-	+	-	+	40%	-	±	(+/-)	(-/+)	+	-	(+/-)			H3K27M突变型	Ⅳ
P6	+		-			+	80%	-	-	+	+	+	弱+	-			野生型	Ⅳ
P7	-		-	+	-	+	30%	-	-	+	散在+	+	-	-			野生型	Ⅳ
P8	+		-			+	80%		±	+	+	+	-	散在+		R132H(-)	野生型	Ⅳ
P9	+	VE1(-)	血管+	-	-	+	45%		<5%	+	野生型	+	+	+			野生型	Ⅳ
P10	+	VE1(-)	-	+	-	+	40%	-	+,约40%	+	+	+	-	-		R132H(-)	野生型	Ⅳ
P11	-	VE1(-)	-	+	-	局灶+	70%	-	±	-	弥漫强+	局灶+	-	+			胶质母细胞瘤	Ⅳ
P12	+		-		-	灶+	60%	-	-	+	+,突变型表达	+	小灶+	-			野生型	Ⅳ
P13		VE1(-)	显示血管增生	+	-	+	60%	-	+,约5%	+	弥漫+，突变型表达	+	-	-			IDH1/2野生型	Ⅳ
P14	+		+	+	局部+	+	+，局部约35%	-	-	局部+	-	+	-	+			野生型	Ⅳ
P15	+		-		-	+	60%	-	-	+	弥漫强+	+	-	+			野生型	Ⅳ
P16	+	VE1(-)	-	+	-	+	+,15%	-	-	+	+	+	-	+		R132H(-)	野生型	Ⅳ
P17	-		-		±	+	40%	+	+,15%	+	+	+	-	+			IDH1突变型	Ⅳ
P18	+	VE1(-)	-	-	-	+	30%	+	-	+	+	+	-	+			野生型	Ⅳ
P19	-	VE1(-)	-	-	-	+	30%	-	-	+	散在+	+	局部+	+			野生型	Ⅳ
P20	+	VE1(-)	-	+	-	-	50%	-	-	+	灶+	+	-	+		R132H(-)	野生型	Ⅳ

基因	位点	改变组表达量	非改变组表达量	Log Ratio	P值	Q值	高表达
MSH2	2p21-p16.3	0.23	0.06	0.17	<0.001	<0.001	改变组
INPP4B	4q31.21	-0.09	0.15	-0.24	<0.001	<0.001	非改变组
ERRFI1	1p36.23	0.15	0.05	0.10	<0.001	<0.001	改变组
XBPI	22q12.l\|22q12	-0.25	0.16	-0.41	<0.001	<0.001	非改变组
AXL	19q13.2	-0.23	-0.01	-0.22	<0.001	<0.001	非改变组
CTNNBI	3p22.1	0.11	-0.08	0.18	<0.001	<0.001	改变组
SERPINE1	7q22.1	1.15	0.21	0.93	<0.001	0.003	改变组
FOXM1	12p13.33	0.20	0.01	0.10	<0.001	0.004	改变组
RAD50	5q31.1	0.06	-0.01	0.07	<0.001	0.004	改变组

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