The Antidiabetic Drug Metformin Inhibits the Proliferation of Bladder Cancer Cells in Vitro and in Vivo

AbstractBladder cancer is one of the most commonly diagnosed malignant tumors in the urinary system and causes a massive cancer-related death. DEPDC1B is a DEP domain-containing protein that has been found to be associated with a variety of human cancers. This study aimed to explore the role and mechanism of DEPDC1B in the development of bladder cancer. The analysis of clinical specimens revealed the upregulated expression of DEPDC1B in bladder cancer, which was positively related to tumor grade. In vitro and in vivo studies showed that DEPDC1B knockdown could inhibit the growth of bladder cancer cells or xenografts in mice. The suppression of bladder cancer by DEPDC1B was executed through inhibiting cell proliferation, cell migration, and promoting cell apoptosis. Moreover, a mechanistic study found that SHC1 may be an important route through which DEPDC1B regulates the development of bladder cancer. Knockdown of SHC1 in DEPDC1B-overexpressed cancer cells could abolish the promotion effects induced by DEPDC1B. In conclusion, DEPDC1B was identified as a key regulator in the development of bladder cancer, which may be used as a potential therapeutic target in the treatment of bladder cancer.

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In vitro and in vivo effects of HAL on porphyrin production in rat bladder cancer cells (AY27)

Journal of Porphyrins and Phthalocyanines ◽

10.1142/s1088424619500615 ◽

2019 ◽

Vol 23 (07n08) ◽

pp. 813-820

Author(s):

Odrun A. Gederaas ◽

Harald Husebye ◽

Anders Johnsson ◽

Susan Callaghan ◽

Anders Brunsvik

Keyword(s):

Bladder Cancer ◽

Cancer Cells ◽

Aminolevulinic Acid ◽

Protoporphyrin Ix ◽

Active Agent ◽

Laser Scanning Microscopy ◽

Rat Bladder ◽

Bladder Cancer Cells

Aminolevulinic acid and hexyl-aminolevulinate serve as biological precursors to produce photosensitive porphyrins in cells via the heme biosynthetic pathway. This pathway is integral to porphyrin-based photodynamic diagnosis and therapy. By adding exogenous hexyl-aminolevulinate to rat bladder cancer cells (AY27, in vitro) and an animal bladder cancer model (in vivo), fluorescent endogenous porphyrin production was stimulated. Lipophilic protoporphyrin IX was identified as the dominant species by reverse high-pressure liquid chromatography. Subcellular porphyrin localization in the AY27 cells was evaluated by confocal laser scanning microscopy and showed almost quantitative bleaching after 20 s. From this study, we ascertained that the protocol described herein is suitable for hexyl-aminolevulinate-mediated photodynamic therapy and diagnosis when protoporphyrin IX is the active agent.

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CALCIUM IONOPHORE, IONOMYCIN INHIBITS GROWTH OF HUMAN BLADDER CANCER CELLS BOTH IN VITRO AND IN VIVO WITH ALTERATION OF BCL-2 AND BAX EXPRESSION LEVELS

The Journal of Urology ◽

10.1097/00005392-199909010-00090 ◽

1999 ◽

Vol 162 (3 Part 1) ◽

pp. 916-921 ◽

Cited By ~ 12

Author(s):

HIDEAKI MIYAKE ◽

ISAO HARA ◽

KAZUKI YAMANAKA ◽

SOICHI ARAKAWA ◽

SADAO KAMIDONO

Keyword(s):

Bladder Cancer ◽

Cancer Cells ◽

Calcium Ionophore ◽

Human Bladder Cancer ◽

Human Bladder ◽

Expression Levels ◽

Bladder Cancer Cells ◽

Human Bladder Cancer Cells

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Short-Term Resveratrol Exposure Causes In Vitro and In Vivo Growth Inhibition and Apoptosis of Bladder Cancer Cells

PLoS ONE ◽

10.1371/journal.pone.0089806 ◽

2014 ◽

Vol 9 (2) ◽

pp. e89806 ◽

Cited By ~ 51

Author(s):

Mo-Li Wu ◽

Hong Li ◽

Li-Jun Yu ◽

Xiao-Yan Chen ◽

Qing-You Kong ◽

...

Keyword(s):

Bladder Cancer ◽

Growth Inhibition ◽

Cancer Cells ◽

Short Term ◽

Bladder Cancer Cells ◽

In Vivo Growth

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The lncRNA DLX6-AS1 promoted cell proliferation, invasion, migration and epithelial-to-mesenchymal transition in bladder cancer via modulating Wnt/β-catenin signaling pathway

Cancer Cell International ◽

10.1186/s12935-019-1010-z ◽

2019 ◽

Vol 19 (1) ◽

Cited By ~ 4

Author(s):

Jinan Guo ◽

Zhixin Chen ◽

Hongtao Jiang ◽

Zhou Yu ◽

Junming Peng ◽

...

Keyword(s):

Cell Proliferation ◽

Bladder Cancer ◽

Cancer Cells ◽

Cancer Cell ◽

Cancer Progression ◽

Bladder Cancer Cell ◽

Mesenchymal Transition ◽

Bladder Cancer Cells

Abstract Background Bladder cancer is the most common human urological malignancies with poor prognosis, and the pathophysiology of bladder cancer involves multi-linkages of regulatory networks in the bladder cancer cells. Recently, the long noncoding RNAs (lncRNAs) have been extensively studied for their role on bladder cancer progression. In this study, we evaluated the expression of DLX6 Antisense RNA 1 (DLX6-AS1) in the cancerous bladder tissues and studied the possible mechanisms of DLX6-AS1 in regulating bladder cancer progression. Methods Gene expression was determined by qRT-PCR; protein expression levels were evaluated by western blot assay; in vitro functional assays were used to determine cell proliferation, invasion and migration; nude mice were used to establish the tumor xenograft model. Results Our results showed the up-regulation of DLX6-AS1 in cancerous bladder cancer tissues and bladder cell lines, and high expression of DLX6-AS1 was correlated with advance TNM stage, lymphatic node metastasis and distant metastasis. The in vitro experimental data showed that DLX6-AS1 overexpression promoted bladder cancer cell growth, proliferation, invasion, migration and epithelial-to-mesenchymal transition (EMT); while DLX6-AS1 inhibition exerted tumor suppressive actions on bladder cancer cells. Further results showed that DLX6-AS1 overexpression increased the activity of Wnt/β-catenin signaling, and the oncogenic role of DLX6-AS1 in bladder cancer cells was abolished by the presence of XAV939. On the other hand, DLX6-AS1 knockdown suppressed the activity of Wnt/β-catenin signaling, and the tumor-suppressive effects of DLX6-AS1 knockdown partially attenuated by lithium chloride and SB-216763 pretreatment. The in vivo tumor growth study showed that DLX6-AS1 knockdown suppressed tumor growth of T24 cells and suppressed EMT and Wnt/β-catenin signaling in the tumor tissues. Conclusion Collectively, the present study for the first time identified the up-regulation of DLX6-AS1 in clinical bladder cancer tissues and in bladder cancer cell lines. The results from in vitro and in vivo assays implied that DLX6-AS1 exerted enhanced effects on bladder cancer cell proliferation, invasion and migration partly via modulating EMT and the activity of Wnt/β-catenin signaling pathway.

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Fiber-modified adenovirus-mediated suicide gene therapy can efficiently eliminate bladder cancer cells in vitro and in vivo

Oncotarget ◽

10.18632/oncotarget.12324 ◽

2016 ◽

Vol 7 (44) ◽

pp. 71710-71717 ◽

Cited By ~ 2

Author(s):

De-Gui Wang ◽

Mei-Jun Zhao ◽

Yong-Qiang Liu ◽

Xiang-Wen Liu ◽

Hai-Tao Niu ◽

...

Keyword(s):

Gene Therapy ◽

Bladder Cancer ◽

Cancer Cells ◽

Suicide Gene ◽

Suicide Gene Therapy ◽

Bladder Cancer Cells

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Circular RNA circGLIS3 promotes bladder cancer proliferation via the miR-1273f/SKP1/Cyclin D1 axis

Cell Biology and Toxicology ◽

10.1007/s10565-021-09591-3 ◽

2021 ◽

Author(s):

Shuilian Wu ◽

Jialei Yang ◽

Haotian Xu ◽

Xin Wang ◽

Ruirui Zhang ◽

...

Keyword(s):

Cell Cycle ◽

Bladder Cancer ◽

Cyclin D1 ◽

Cancer Cells ◽

Cancer Progression ◽

Migration And Invasion ◽

Multiple Tumor ◽

Bladder Cancer Cells

AbstractExtensive research confirmed that circRNA can play a regulatory role in various stages of tumors by interacting with various molecules. Identifying the differentially expressed circRNA in bladder cancer and exploring its regulatory mechanism on bladder cancer progression are urgent. In this study, we screened out a circRNA-circGLIS3 with a significant upregulation trend in both bladder cancer tissues and cells. Bioinformatics prediction results showed that circGLIS3 may be involved in multiple tumor-related pathways. Function gain and loss experiments verified circGLIS3 can affect the proliferation, migration, and invasion of bladder cancer cells in vitro. Moreover, silencing circGLIS3 inhibited bladder cancer cell growth in vivo. Subsequent research results indicated circGLIS3 regulated the expression of cyclin D1, a cell cycle–related protein, and cell cycle progression. Mechanically, circGLIS3 upregulates the expression of SKP1 by adsorbing miR-1273f and then promotes cyclin D1 expression, ultimately promoting the proliferation of bladder cancer cells. In summary, our study indicates that circGLIS3 plays an oncogene role in the development of bladder cancer and has potential to be a candidate for bladder cancer. Graphical abstract

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Nanaomycin K inhibited epithelial mesenchymal transition and tumor growth in bladder cancer cells in vitro and in vivo

Scientific Reports ◽

10.1038/s41598-021-88741-3 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Koichi Kitagawa ◽

Katsumi Shigemura ◽

Aya Ishii ◽

Takuji Nakashima ◽

Hirotaka Matsuo ◽

...

Keyword(s):

Bladder Cancer ◽

Cancer Cells ◽

Epithelial Mesenchymal Transition ◽

Mesenchymal Transition ◽

Invasion And Migration ◽

Bladder Cancer Cells ◽

And Migration ◽

Muscle Invasive

AbstractNanaomycin K, derived from Streptomyces rosa subsp. notoensis OS-3966T, has been discovered to have inhibitory bioactivity on epithelial–mesenchymal transition (EMT), an important mechanism of cancer cell invasion and migration. In this study, we examined the anti-EMT and anti-tumor effect of nanaomycin K in bladder cancer, where EMT has important roles in progression. We treated two bladder cancer lines, non-muscle-invasive KK47 and muscle-invasive T24, with nanaomycin K to determine the effects on cell proliferation, apoptosis and expression of EMT markers in vitro. Wound-healing assays were performed to assess cell invasion and migration. We conducted an in vivo xenograft study in which mice were inoculated with bladder cancer cells and treated with intratumoral administration of nanaomycin K to investigate its anti-tumor and EMT inhibition effects. As the results, nanaomycin K (50 µg/mL) significantly inhibited cell proliferation in KK47 (p < 0.01) and T24 (p < 0.01) in the presence of TGF-β, which is an EMT-inducer. Nanaomycin K (50 µg/mL) also significantly inhibited cell migration in KK47 (p < 0.01) and T24 (p < 0.01), and induced apoptosis in both cell lines in the presence of TGF-β (p < 0.01). Nanaomycin K increased the expression of E-cadherin and inhibited the expression of N-cadherin and vimentin in both cell lines. Nanaomycin K also decreased expression of Snail, Slug, phospho-p38 and phospho-SAPK/JNK especially in T24. Intratumoral administration of nanaomycin K significantly inhibited tumor growth in both KK47 and T24 cells at high dose (1.0 mg/body) (p = 0.009 and p = 0.003, respectively) with no obvious adverse events. In addition, nanaomycin K reversed EMT and significantly inhibited the expression of Ki-67 especially in T24. In conclusion, we demonstrated that nanaomycin K had significant anti-EMT and anti-tumor effects in bladder cancer cells, suggesting that nanaomycin K may be a therapeutic candidate for bladder cancer treatment.

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