KIAA1522对肺癌细胞增殖、迁移和侵袭的影响及其机制

doi:10.13481/j.1671-587X.20250317

吉林大学学报(医学版) ›› 2025, Vol. 51 ›› Issue (3): 727-739.doi: 10.13481/j.1671-587X.20250317

• 临床研究 • 上一篇

KIAA1522对肺癌细胞增殖、迁移和侵袭的影响及其机制

王艺慧¹,张晴¹,李英楠¹,叶丽平^1,^2,³()

^1.锦州医科大学基础医学院病理生理学教研室，辽宁锦州 121001
^2.锦州医科大学生物人类学研究所，辽宁锦州 121001
^3.锦州医科大学辽宁省人类表型组学研究重点实验室，辽宁锦州 121001

收稿日期:2024-06-12 接受日期:2024-08-06 出版日期:2025-05-28 发布日期:2025-07-18
通讯作者: 叶丽平 E-mail:yeliping@jzmu.edu.cn
作者简介:王艺慧（1996-），女，山东省泰安市人，医学硕士，主要从事肿瘤侵袭转移和机制方面的研究。
基金资助:
吴阶平医学基金会研究基金项目(320.6750.2020-06-68)

Effect of KIAA1522 on proliferation, migration, and invasion of lung cancer cells and its mechanism

Yihui WANG¹,Qing ZHANG¹,Yingnan LI¹,Liping YE^1,^2,³()

^1.Department of Pathophysiology，School of Basic Medical Sciences，Jinzhou Medical University，Jinzhou 121001，China
^2.Institute of Biological Anthropology，Jinzhou Medical University，Jinzhou 121001，China
^3.Liaoning Provincal Key Laboratory of Human Phenome Research，Jinzhou Medical University，Jinzhou 121001，China

Received:2024-06-12 Accepted:2024-08-06 Online:2025-05-28 Published:2025-07-18
Contact: Liping YE E-mail:yeliping@jzmu.edu.cn

摘要/Abstract

摘要：

目的探讨KIAA1522对肺癌细胞增殖、迁移和侵袭的影响，并阐明其信号机制。方法采用生物信息学方法分析75例人非小细胞肺癌（NSCLC）组织和癌旁正常肺组织中KIAA1522 mRNA及蛋白表达水平，免疫组织化学染色法检测NSCLC组织及癌旁正常肺组织中KIAA1522蛋白表达情况，Western blotting法检测在多种肺癌细胞系中KIAA1522蛋白表达水平。分别将KIAA1522-小干扰RNA（siRNA）和过表达质粒转染至肺癌H1299及A549细胞。KIAA1522-siRNA实验分为空白组、阴性对照组（si-NC组）、KIAA1522-siRNA#1组和KIAA1522-siRNA#2组；KIAA1522过表达实验分为对照组、空载对照组（OE-NC组，转染KIAA1522过表达空载质粒）、过表达KIAA1522组（OE-KIAA1522组，转染KIAA1522过表达质粒）、过表达KIAA1522+MK2206组［OE-KIAA1522+MK2206组，共转染KIAA1522过表达质粒和蛋白激酶B（AKT）信号通路抑制剂MK2206］和MK2206组（转染MK2206）。采用Western blotting法验证各组细胞转染效率，噻唑蓝（MTT）法检测各组肺癌细胞增殖活性，细胞划痕实验检测各组肺癌细胞迁移率，Transwell小室实验检测各组肺癌细胞中侵袭细胞数，Western blotting法检测各组细胞中磷酸化AKT（p-AKT）、总AKT（t-AKT）、细胞周期蛋白D1（Cyclin D1）、血管内皮生长因子（VEGF）和上皮-间质转化（EMT）相关蛋白［波形蛋白（Vimentin）、N钙黏蛋白（N-cadherin）和E钙黏蛋白（E-cadherin）］蛋白表达水平。结果生物信息学方法分析，与癌旁正常肺组织比较，NSCLC组织中KIAA1522 mRNA和蛋白表达水平均明显升高（P<0.05或P<0.01）。免疫组织化学染色法，与癌旁正常肺组织比较，NSCLC组织中KIAA1522蛋白阳性表达率明显升高（P<0.05），且与TNM分期有关（P<0.01）。Western blotting法，与正常肺上皮细胞BEAS-2B比较，肺癌细胞系PC9、H1299、H460、A549、H1975和H226细胞中KIAA1522蛋白表达水平均明显升高（P<0.05或P<0.01）。与si-NC组比较，KIAA1522-siRNA#1组和KIAA1522-siRNA#2组H1299细胞中KIAA1522蛋白表达水平均明显降低（P<0.01）；与OE-NC组比较，OE-KIAA1522组A549细胞中KIAA1522蛋白表达水平明显升高（P<0.01）。MTT法，细胞培养24、48和72 h时，与si-NC组比较，KIAA1522-siRNA#1组和KIAA1522-siRNA#2组H1299细胞增殖活性均明显降低（P<0.01）；与OE-NC组比较，OE-KIAA1522组A549细胞增殖活性明显升高（P<0.05）；与OE-KIAA1522组比较，OE-KIAA1522+MK2206组A549细胞增殖活性明显降低（P<0.01）；与OE-KIAA1522+MK2206组比较，MK2206组A549细胞增殖活性明显降低（P<0.05）。细胞划痕实验，与si-NC组比较，KIAA1522-siRNA#1组和KIAA1522-siRNA#2组H1299细胞迁移率均明显降低（P<0.01）；与OE-NC组比较，OE-KIAA1522组A549细胞迁移率明显升高（P<0.01）；与OE-KIAA1522组比较，OE-KIAA1522+MK2206组A549细胞迁移率明显降低（P<0.05）；与OE-KIAA1522+MK2206组比较，MK2206组A549细胞迁移率明显降低（P<0.05）。Transwell小室实验，与si-NC组比较，KIAA1522-siRNA#1组和KIAA1522-siRNA#2组H1299细胞中侵袭细胞数明显减少（P<0.01）；与OE-NC组比较，OE-KIAA1522组A549细胞侵袭细胞数明显增多（P<0.01）；与OE-KIAA1522组比较，OE-KIAA1522+MK2206组A549细胞中侵袭细胞数明显减少（P<0.01）；与OE-KIAA1522+MK2206组比较，MK2206组A549细胞中侵袭细胞数明显减少（P<0.01）。Western blotting法，与si-NC组比较，KIAA1522-siRNA#1组和KIAA1522-siRNA#2组H1299细胞中p-AKT、Cyclin D1、Vimentin、N-cadherin及VEGF蛋白表达水平均明显降低（P<0.05或P<0.01），E-cadherin蛋白表达水平明显升高（P<0.01）；与OE-NC组比较，OE-KIAA1522组A549细胞中p-AKT、Cyclin D1、Vimentin、N-cadherin和VEGF蛋白表达水平均明显升高（P<0.05或P<0.01），E-cadherin蛋白表达水平明显降低（P<0.05）；与OE-KIAA1522组比较，OE-KIAA1522+MK2206组A549细胞中p-AKT、Cyclin D1、Vimentin、N-cadherin和VEGF蛋白表达水平均明显降低（P<0.05或P<0.01），E-cadherin蛋白表达水平明显升高（P<0.05）；与OE-KIAA1522+MK2206组比较，MK2206组A549细胞中Cyclin D1、Vimentin、N-cadherin和VEGF蛋白表达水平均明显降低（P<0.05或P<0.01），E-cadherin蛋白表达水平明显升高（P<0.05）。结论 KIAA1522蛋白可上调肺癌细胞中Cyclin D1、EMT相关蛋白和VEGF蛋白表达，促进肺癌细胞的增殖、迁移和侵袭，其作用机制与激活AKT信号通路有关。

关键词: KIAA1522, 癌，非小细胞肺, 蛋白激酶B, 细胞增殖, 细胞侵袭

Abstract:

Objective To discuss the effect of KIAA1522 on the proliferation， migration， and invasion of lung cancer cells， and to clarify its signaling mechanism. Methods Bioinformatics analysis was used to detect the expression levels of KIAA1522 mRNA and protein in 75 cases of human non-small cell lung cancer （NSCLC） tissues and adjacent normal lung tissues； immunohistochemical staining was used to detect the expression of KIAA1522 protein in NSCLC tissue and adjacent normal lung tissues； Western blotting method was used to detect the expression level of KIAA1522 protein in various lung cancer cell lines. KIAA1522-small interfering（siRNA） and over-expression plasmids were transfected into the lung cancer H1299 and A549 cells， respectively. The KIAA1522-siRNA experiment was divided into blank group， negative control group （si-NC group）， KIAA1522-siRNA#1 group， and KIAA1522-siRNA#2 group. The KIAA1522 over-expression experiment was divided into control group， empty vector control group （OE-NC group， transfected with KIAA1522 over-expression empty vector plasmid）， KIAA1522 overexpression group （OE-KIAA1522 group， transfected with KIAA1522 over-expression plasmid）， KIAA1522 over-expression+MK2206 group ［OE-KIAA1522+MK2206 group， co-transfected with KIAA1522 over-expression plasmid and protein kinase B （AKT） signaling pathway inhibitor MK2206］， and MK2206 group （transfected with MK2206）. Western blotting method was used to verify the transfection efficiencies of the cells in various groups； MTT assay was used to detect the proliferation activities of the lung cancer cells in various groups； cell scratch assay was used to detect the migration rates of lung cancer cells in various groups； Transwell chamber assay was used to detect the numbers of invasion lung cancer cells in various groups； Western blotting method was used to detect the expression levels of phosphorylated AKT （p-AKT）， total AKT （t-AKT）， cyclin D1 （Cyclin D1）， vascular endothelial growth factor （VEGF）， and epithelial-mesenchymal transition （EMT）-related proteins ［vimentin （Vimentin）， N-cadherin （N-cadherin）， and E-cadherin （E-cadherin）］ proteins in the cells in various groups. Results The bioinformatics analysis results showed that compared with adjacent normal lung tissue， the expression levels of KIAA1522 mRNA and protein in NSCLC tissue were significantly increased （P<0.05 or P<0.01）. The immunohistochemistry staining results showed that compared with adjacent normal lung tissue， the positive expression rate of KIAA1522 protein in NSCLC tissue was significantly increased （P<0.05） and was associated with TNM stage （P<0.01）. The Western blotting results showed that compared with normal lung epithelial cells BEAS-2B， the expression levels of KIAA1522 protein in lung cancer cell lines PC9， H1299， H460， A549， H1975， and H226 were significantly increased （P<0.05 or P<0.01）. Compared with si-NC group， the expression levels of KIAA1522 protein in the H1299 cells in KIAA1522-siRNA#1 group and KIAA1522-siRNA#2 group were significantly decreased （P<0.01）； compared with OE-NC group， the expression level of KIAA1522 protein in the A549 cells in OE-KIAA1522 group was significantly increased （P<0.01）. The MTT results showed that at 24， 48， and 72 h of cell culture， compared with si-NC group， the proliferation activities of the H1299 cells in KIAA1522-siRNA#1 group and KIAA1522-siRNA#2 group were significantly decreased （P<0.01）； compared with OE-NC group， the proliferation activity of the A549 cells in OE-KIAA1522 group was significantly increased （P<0.05）； compared with OE-KIAA1522 group， the proliferation activity of the A549 cells in OE-KIAA1522+MK2206 group was significantly decreased （P<0.01）； compared with OE-KIAA1522+MK2206 group， the proliferation activity of the A549 cells in MK2206 group was significantly decreased （P<0.05）. The cell scratch assay results showed that compared with si-NC group， the migration rates of the H1299 cells in KIAA1522-siRNA#1 group and KIAA1522-siRNA#2 group were significantly decreased （P<0.01）； compared with OE-NC group， the migration rate of the A549 cells in OE-KIAA1522 group was significantly increased （P<0.01）； compared with OE-KIAA1522 group， the migration rate of the A549 cells in OE-KIAA1522+MK2206 group was significantly decreased （P<0.05）； compared with OE-KIAA1522+MK2206 group， the migration rate of the A549 cells in MK2206 group was significantly decreased （P<0.05）. The Transwell chamber assay results showed that compared with si-NC group， the numbers of invasion H1299 cells in KIAA1522-siRNA#1 group and KIAA1522-siRNA#2 group were significantly decreased （P<0.01）； compared with OE-NC group， the number of invasion A549 cells in OE-KIAA1522 group was significantly increased （P<0.01）； compared with OE-KIAA1522 group， the number of invasion A549 cells in OE-KIAA1522+MK2206 group was significantly decreased （P<0.01）； compared with OE-KIAA1522+MK2206 group， the number of invasion A549 cells in MK2206 group was significantly decreased （P<0.01）. The Western blotting results showed that compared with si-NC group， the expression levels of p-AKT， Cyclin D1， Vimentin， N-cadherin， and VEGF proteins in the H1299 cells in KIAA1522-siRNA#1 group and KIAA1522-siRNA#2 group were significantly decreased （P<0.05 or P<0.01）， while the expression level of E-cadherin protein was significantly increased （P<0.01）； compared with OE-NC group， the expression levels of p-AKT， Cyclin D1， Vimentin， N-cadherin， and VEGF proteins in the A549 cells in OE-KIAA1522 group were significantly increased （P<0.05 or P<0.01）， while the expression level of E-cadherin protein was significantly decreased （P<0.05）； compared with OE-KIAA1522 group， the expression levels of p-AKT， Cyclin D1， Vimentin， N-cadherin， and VEGF proteins in the A549 cells in OE-KIAA1522+MK2206 group were significantly decreased （P<0.05 or P<0.01）， while the expression level of E-cadherin protein was significantly increased （P<0.05）； compared with OE-KIAA1522+MK2206 group， the expression levels of Cyclin D1， Vimentin， N-cadherin， and VEGF proteins in the A549 cells in MK2206 group were significantly decreased （P<0.05 or P<0.01）， while the expression level of E-cadherin protein was significantly increased （P<0.05）. Conclusion The KIAA1522 protein upregulates the expression of Cyclin D1， EMT-related proteins， and VEGF protein in lung cancer cells， promoting the proliferation， migration， and invasion of lung cancer cells， and its mechanism is related to the activation of the AKT signaling pathway.

Key words: KKIAA1522, Carcinoma， non-small-cell lung, Protein kinase B, Cell proliferation, Cell invasion

中图分类号:

R734.2

王艺慧,张晴,李英楠,叶丽平. KIAA1522对肺癌细胞增殖、迁移和侵袭的影响及其机制[J]. 吉林大学学报(医学版), 2025, 51(3): 727-739.

Yihui WANG,Qing ZHANG,Yingnan LI,Liping YE. Effect of KIAA1522 on proliferation, migration, and invasion of lung cancer cells and its mechanism[J]. Journal of Jilin University(Medicine Edition), 2025, 51(3): 727-739.

图/表 13

图1

图2

表1

不同临床病理特征 NSCLC 患者癌组织中KIAA1522蛋白表达情况"

Clinicopathological characteristic	n	KIAA1522		$χ 2$	P
Clinicopathological characteristic	n	＋	－	$χ 2$	P
Age
≤60	33	26	7	0.251	0.616
>60	42	31	11	0.251	0.616
Gender
Male	43	32	11	0.488	0.485
Female	32	26	6	0.488	0.485
Maximum diameter of tumor（cm）
≤3	34	24	10	1.614	0.204
>3	41	34	7	1.614	0.204
Differentiation
Well-moderate	51	42	9	2.291	0.130
Poor	24	16	8	2.291	0.130
TNM stage
Ⅰ	31	18	13	11.192	0.001
Ⅱ+Ⅲ	44	40	4	11.192	0.001
Lymphnode metastasis
Yes	2	2	0		1.000
No	73	56	17	-	1.000

表1

图3

图4

图5

表2

表3

图6

图7

图8

图9

图10

参考文献 25

[1]	ZHANG X， ZHANG R， LIU P P， et al. ATP8B1 knockdown activated the choline metabolism pathway and induced high-level intracellular REDOX homeostasis in lung squamous cell carcinoma［J］. Cancers （Basel）， 2022， 14（3）： 835.
[2]	YANG D W， LIU Y， BAI C X， et al. Epidemiology of lung cancer and lung cancer screening programs in China and the United States［J］. Cancer Lett， 2020， 468： 82-87.
[3]	解智慧. 一种新的介导细胞间粘附的肌动蛋白相关蛋白KIAA1522在食管癌中作用及其机制的研究［D］. 北京：北京协和医学院， 2014.
[4]	XU Y Z， SUN C D， HAN B， et al. High KIAA1522 expression predicts a poor prognosis in patients with hepatocellular carcinoma［J］. Oncol Lett， 2020， 20（1）： 509-516.
[5]	SHI Y J， XIAO Q W， HUANG S C， et al. Poor prognostic biomarker KIAA1522 is associated with immune infiltrates in hepatocellular carcinoma［J］. J Oncol， 2023， 2023： 3538928.
[6]	ÖZDEDE M， TABAN H K， AKMAN O， et al. The prognostic significance of KIAA1522 expression in non-small-cell lung cancer patients［J］. Cureus， 2023， 15（8）： e44016.
[7]	HU B， YANG X B， YANG X， et al. LncRNA CYTOR affects the proliferation， cell cycle and apoptosis of hepatocellular carcinoma cells by regulating the miR-125b-5p/KIAA1522 axis［J］. Aging （Albany NY）， 2020， 13（2）： 2626-2639.
[8]	JIANG S B， ZHANG Y G， LI Q， et al. KIAA1522 promotes the progression of hepatocellular carcinoma via the activation of the Wnt/β-catenin signaling pathway［J］. Onco Targets Ther， 2020， 13： 5657-5668.
[9]	WANG B S， JING T T， JIN W L， et al. KIAA1522 potentiates TNFα-NFκB signaling to antagonize platinum-based chemotherapy in lung adenocarcinoma［J］. J Exp Clin Cancer Res， 2020， 39（1）： 170.
[10]	YI X， HU C H， ZHANG C， et al. KIAA1522 is a new biomarker of promoting the tumorigenesis and distant metastasis of colorectal carcinoma［J］. Cell Signal， 2022， 90： 110202.
[11]	XIE Z H， YU J， SHANG L， et al. KIAA1522 overexpression promotes tumorigenicity and metastasis of esophageal cancer cells through potentiating the ERK activity［J］. Onco Targets Ther， 2017， 10： 3743-3754.
[12]	HUA H， ZHANG H Y， CHEN J Z， et al. Targeting Akt in cancer for precision therapy［J］. J Hematol Oncol， 2021， 14（1）： 128.
[13]	ZHAO L M， LI J， LIU Y P， et al. Flotillin1 promotes EMT of human small cell lung cancer via TGF-β signaling pathway［J］. Cancer Biol Med， 2018， 15（4）： 400-414.
[14]	KONG D G， ZHOU H B， NEELAKANTAN D， et al. VEGF-C mediates tumor growth and metastasis through promoting EMT-epithelial breast cancer cell crosstalk［J］. Oncogene， 2021， 40（5）： 964-979.
[15]	FAN Y G， JIANG Y， GONG L， et al. Epidemiological and demographic drivers of lung cancer mortality from 1990 to 2019： results from the global burden of disease study 2019［J］. Front Public Health， 2023， 11： 1054200.
[16]	GUO B Q， YU L， SUN Y H， et al. Long non-coding RNA USP2-AS1 accelerates cell proliferation and migration in ovarian cancer by sponging miR-520d-3p and up-regulating KIAA1522［J］. Cancer Manag Res， 2020， 12： 10541-10550.
[17]	LIN J， LIAO S S， LIU Z W， et al. LncRNA FGD5-AS1 accelerates cell proliferation in pancreatic cancer by regulating miR-520a-3p/KIAA1522 axis［J］. Cancer Biol Ther， 2021， 22（3）： 257-266.
[18]	NOWAK E， BEDNAREK I. Aspects of the epigenetic regulation of EMT related to cancer metastasis［J］. Cells， 2021， 10（12）： 3435.
[19]	HUANG Y H， HONG W Q， WEI X W. The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis［J］. J Hematol Oncol， 2022， 15（1）： 129.
[20]	张瑞，陈进宏. 结直肠癌肝转移的非根治性切除手术治疗策略［J］. 临床肝胆病杂志， 2024， 40（7）： 1295-1300.
[21]	RAVAGGI A， GAMBINO A， FERRARI F， et al. VEGF-D serum level as a potential predictor of lymph node metastasis and prognosis in vulvar squamous cell carcinoma patients［J］. Front Oncol， 2022， 12： 818613.
[22]	LI C， WANG H F， FANG H， et al. FOXP3 facilitates the invasion and metastasis of non-small cell lung cancer cells through regulating VEGF， EMT and the Notch1/Hes1 pathway［J］. Exp Ther Med， 2021， 22（3）： 958.
[23]	MAHARATI A， MOGHBELI M. PI3K/AKT signaling pathway as a critical regulator of epithelial-mesenchymal transition in colorectal tumor cells［J］. Cell Commun Signal， 2023， 21（1）： 201.
[24]	ZHENG Y H， JI H X， YI W L， et al. PRMT5 facilitates angiogenesis and EMT via HIF-1α/VEGFR/Akt signaling axis in lung cancer［J］. Aging （Albany NY）， 2023， 15（13）： 6163-6178.
[25]	HAN P， WANG Q L， ZHANG X. Expression of TRAP1 in gastric cancer tissue and its correlation with malignant biology［J］. Asian Pac J Trop Med， 2016， 9（1）： 67-71.

Group	Proliferation activity
Group	（t/h）	24	48	72
Si-NC		0.146±0.008	0.200±0.009	0.278±0.010
KIAA1522-siRNA#1		0.095±0.010^*	0.161±0.001^*	0.224±0.007^*
KIAA1522-siRNA#2		0.089±0.010^*	0.156±0.011^*	0.204±0.004^*

Group	Proliferation activity
Group	（t/h）	24	48	72
OE-NC		0.138±0.012	0.216±0.006	0.330±0.007
OE-KIAA1522		0.150±0.016^*	0.255±0.014^*	0.388±0.011^*
OE-KIAA1522+MK2206		0.129±0.007^△	0.191±0.013^△	0.300±0.012^△
MK2206		0.118±0.011^#	0.158±0.007^#	0.261±0.004^#

KIAA1522对肺癌细胞增殖、迁移和侵袭的影响及其机制

Effect of KIAA1522 on proliferation, migration, and invasion of lung cancer cells and its mechanism

RichHTML

PDF (PC)

赞

可视化

摘要/Abstract

引用本文

使用本文

图/表 13

参考文献 25

相关文章 15

Metrics

本文评价

推荐阅读 0

[1]	陈程,李警耀,胡万祥,刘东慧,陈志宏. 丝胶通过Akt1调控PI3K/Akt/NF-κB信号通路对链脲佐菌素引起INS-1细胞损伤的保护作用及其机制[J]. 吉林大学学报(医学版), 2025, 51(3): 590-598.
[2]	王繁,温馨,王艺璇,王远. 缝隙连接蛋白β2对肺腺癌患者预后及肺腺癌A549细胞生物学行为的影响[J]. 吉林大学学报(医学版), 2025, 51(3): 716-726.
[3]	孙淑妍,张华坤,周紫如,李锋,崔晓宾. 食管鳞状细胞癌组织中CRNN蛋白的表达及其过表达对食管鳞状细胞癌Eca9706细胞生物学行为的影响[J]. 吉林大学学报(医学版), 2025, 51(2): 275-283.
[4]	卢梦云,韩语诚,胡溢洪,何旻蕙,张艳群,邹先琼. 糖脂转运蛋白对胰腺癌PANC-1细胞增殖、迁移和侵袭的影响及其机制[J]. 吉林大学学报(医学版), 2025, 51(2): 284-295.
[5]	邓静,王萱,石长玉,杨斯琦,邹亲玲,金明. 一叶秋碱对人结肠癌SW620细胞增殖和凋亡的影响及其机制[J]. 吉林大学学报(医学版), 2025, 51(2): 307-316.
[6]	杨英,赵亮,由涌,许倩,杨振军. 17β-雌二醇对海马神经干细胞增殖和分化的影响及其机制[J]. 吉林大学学报(医学版), 2025, 51(2): 317-324.
[7]	王妍,赵邹宇,于盼盼,杨萍. IκB激酶相互作用蛋白在宫颈癌组织中的表达及其对宫颈癌细胞增殖、迁移和侵袭的影响[J]. 吉林大学学报(医学版), 2025, 51(2): 341-351.
[8]	张雅琪,米靖,杨景荣,李欣明,李利. 上调miR-31表达通过Wnt/β-catenin信号通路对牙髓干细胞成骨分化的影响[J]. 吉林大学学报(医学版), 2025, 51(2): 412-419.
[9]	张潮鹤,张昕玮,王相峰. 片仔癀在对乙酰氨基酚所致肝损伤中的保护作用及其机制[J]. 吉林大学学报(医学版), 2025, 51(1): 105-114.
[10]	武鹏立,李凤玉,刘博,吕洋. 沉默DDX39A基因对食管癌TE-1细胞增殖、迁移和侵袭的作用及其机制[J]. 吉林大学学报(医学版), 2025, 51(1): 115-123.
[11]	赵蒙蒙,王雅璐,许宇翔,杨凯歌,曹玉文,周文虎,费晶,王雯,罗成华,胡建明. 硫化氢合成酶CBS和CSE对乳腺癌细胞恶性生物学行为的影响[J]. 吉林大学学报(医学版), 2025, 51(1): 34-43.
[12]	杨露,傅家财,李凤金,齐玲. 五味子乙素对胰腺癌细胞迁移和侵袭的抑制作用及其机制[J]. 吉林大学学报(医学版), 2025, 51(1): 44-50.
[13]	赵芳,李珍玲,朴丽花,韩龙哲,崔银姬,权春姬,金雪梅. Yes相关蛋白对人宫颈癌SiHa细胞生物学行为的影响[J]. 吉林大学学报(医学版), 2025, 51(1): 68-75.
[14]	陈敏,朱慧艳,陶静,徐奕鹏. 甜菜碱对大鼠脑微血管内皮细胞氧糖剥夺损伤的改善作用及对PI3K/AKT通路的影响[J]. 吉林大学学报(医学版), 2025, 51(1): 96-104.
[15]	孙高,何静,赵琪,石剑虹,廖智羚,田原野,吴国民. 白藜芦醇对颞下颌关节骨关节炎的治疗作用及其机制[J]. 吉林大学学报(医学版), 2024, 50(6): 1547-1556.