Expression of a tumor-associated gene, LASS2, in the human bladder carcinoma cell lines BIU-87, T24, EJ and EJ-M3

Zhao, Qinghua; Wang, Haifeng; Mingying, Yang; Yang, Delin; Zuo, Yigang; Wang, Jiansong

doi:10.3892/etm.2013.892

Cited by 18 publications

(20 citation statements)

References 20 publications

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“…Our previous study demonstrated that LASS2-negative bladder cancer was associated with poor clinical prognosis [29]. LASS2 downregulation leads to enhanced ability of proliferation and invasion in bladder cancer cells [30]. In addition, LASS2 enhances chemosensitivity of breast cancer by counteracting acidic tumor microenvironment through inhibiting activity of VATPase proton pump and IAP signaling pathway [19], which suggests LASS2 may regulate Bcl-2 and survivin expression.…”

Section: Discussionmentioning

confidence: 98%

miR-9 promotes cell proliferation and inhibits apoptosis by targeting LASS2 in bladder cancer

et al. 2015

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MicroRNA-9 upregulation was reported in several tumors. However, its function and mechanism in human bladder cancer remains obscure. The present study aims to identify the expression pattern, biological roles and potential mechanism of miR-9 in human bladder cancers. We found that expression level of miR-9 in bladder cancer tissues was higher than normal tissues. miR-9 mimic transfection was performed in T24 and 5637 cells with low miR-9 expression, and miR-9 inhibitor was employed in BIU-87 cell line with high endogenous expression. miR-9 increased cell proliferation, cell cycle progression, invasion and chemoresistance, with upregulation of cyclin D1, MMP9, Bcl-2, and survivin and downregulation of E-cadherin. Using luciferase reporter assay, we confirmed that LASS2 was a direct target of miR-9 in bladder cancer cells. Transfection of miR-9 mimic downregulated LASS2 expression. LASS2 transfection downregulated Bcl-2 and survivin expression, which were induced by miR-9 mimic in both cell lines. In conclusion, these results indicate that miR-9 upregulation might be associated with malignant phenotype of bladder cancer. miR-9 promotes chemoresistance of bladder cancer cells by target LASS2.

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Section: Discussionmentioning

confidence: 98%

miR-9 promotes cell proliferation and inhibits apoptosis by targeting LASS2 in bladder cancer

et al. 2015

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“…RT-qPCR was conducted according to previously described methods ( 11 ). Briefly, total mRNA was extracted using TRIzol (Invitrogen) and purified.…”

Section: Methodsmentioning

confidence: 99%

“…Western blot assays were performed according to previously described methods ( 10 , 11 , 13 ). Briefly, cMSCs were lysed with RIPA buffer containing phenylmethylsulfonyl fluoride (Sangon Biotech Co., Ltd.), then 50 µg total protein was quantitated using a BCA protein assay kit (P0009; Beyotime Institute of Biotechnology) and subjected to 6–10% SDS-PAGE.…”

Section: Methodsmentioning

confidence: 99%

Electric pulse current stimulation increases electrophysiological properties of If current reconstructed in mHCN4-transfected canine mesenchymal stem cells

Yang

Luo

Pan

et al. 2016

Experimental and Therapeutic Medicine

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The ‘funny’ current, also known as the If current, play a crucial role in the spontaneous diastolic depolarization of sinoatrial node cells. The If current is primarily induced by the protein encoded by the hyperpolarization-activated cyclic nucleotide-gated channel 4 (HCN4) gene. The functional If channel can be reconstructed in canine mesenchymal stem cells (cMSCs) transfected with mouse HCN4 (mHCN4). Biomimetic studies have shown that electric pulse current stimulation (EPCS) can promote cardiogenesis in cMSCs. However, whether EPCS is able to influence the properties of the If current reconstructed in mHCN4-transfected cMSCs remains unclear. The present study aimed to investigate the effects of EPCS on the If current reconstructed in mHCN4-transfected cMSCs. The cMSCs were transfected with the lentiviral vector pLentis-mHCN4-GFP. Following transfection, these cells were divided into two groups: mHCN4-transfected cMSCs (group A), and mHCN4-transfected cMSCs induced by EPCS (group B). Using a whole cell patch-clamp technique, the If current was recorded, and group A cMSCs showed significant time and voltage dependencies and sensitivity to extracellular Cs+. The half-maximal activation (V1/2) value was −101.2±4.6 mV and the time constant of activation was 324±41 msec under −160 mV. In the group B cells the If current increased obviously and activation curve moved to right. The absolute value of V1/2 increased significantly to −92.4±4.8 mV (P<0.05), and the time constant of activation diminished under the same command voltage (251±44 vs. 324±41, P<0.05). In addition, the mRNA and protein expression levels of HCN4, connexin 43 (Cx43) and Cx45 were upregulated in group B compared with group A, as determined by reverse transcription-quantitative polymerase chain reaction and western blot analyses. Transmission electron micrographs also confirmed the increased gap junctions in group B. Collectively, these results indicated that reconstructed If channels may have a positive regulatory role in EPCS induction. The cMSCs transfected with mHCN4 induced by EPCS may be a source of effective biological pacemaker cells.

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“…In previous studies, an implantation metastasis model of the highly invasive human bladder cancer EJ-M3 cell line was established in nude mice ( 11 , 12 ). Another study identified that LASS2 expression was the highest in the EJ-M3 cell line compared with other human bladder carcinoma cell lines (BIU-87, T24 and EJ), and was significantly correlated with the proliferation, metastasis and invasion of human bladder cancer ( 13 ). In the present study, EJ-M3 cells were selected for a lentivirus-mediated LASS2 interference strategy and LASS2 overexpression, in order to investigate the effects of LASS2 expression on bladder cancer cell tumorigenicity and growth in vitro and in nude mice.…”

Section: Introductionmentioning

confidence: 99%

The role of LASS2 in regulating bladder cancer cell tumorigenicity in a nude mouse model

et al. 2017

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Previous in vitro studies have demonstrated that LAG1 longevity assurance homolog 2 (LASS2) is a novel tumor suppressor gene that is significantly associated with the proliferation and invasion ability of tumor cells. However, the role LASS2 serves in regulating bladder cancer cell tumorigenicity and tumor growth in vivo has not yet been elucidated in animal or clinical studies. In the present study, LASS2 knockdown in human bladder cancer EJ-M3 cells significantly promoted the growth of xenografts in nude mice compared with the control group, while overexpression of LASS2 suppressed tumor growth; however, this was not statistically significant. Furthermore, LASS2 knockdown resulted in more apparent heteromorphism and a higher activity of matrix metalloproteinase (MMP)-2 and MMP-9 in xenograft tumors. The data from the present study demonstrated that LASS2 knockdown significantly promoted the tumorigenicity and growth of EJ-M3 xenograft tumors in nude mice, and that LASS2 overexpression has a tendency to inhibit the growth of xenografts, suggesting that it may be a potential therapeutic target for bladder cancer.

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Expression of a tumor-associated gene, LASS2, in the human bladder carcinoma cell lines BIU-87, T24, EJ and EJ-M3

Cited by 18 publications

References 20 publications

miR-9 promotes cell proliferation and inhibits apoptosis by targeting LASS2 in bladder cancer

miR-9 promotes cell proliferation and inhibits apoptosis by targeting LASS2 in bladder cancer

Electric pulse current stimulation increases electrophysiological properties of If current reconstructed in mHCN4-transfected canine mesenchymal stem cells

The role of LASS2 in regulating bladder cancer cell tumorigenicity in a nude mouse model

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