Loss of polarity protein Par3, via transcription factor Snail, promotes bladder cancer metastasis

Wang, Shenyi; Cai, Jinming; Zhang, Si; Dong, Mingwei; Zhang, Li; Xu, Yingying; Shen, Bing; Chen, She

doi:10.1111/cas.14920

Cited by 11 publications

(8 citation statements)

References 39 publications

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“…Moreover, the epidemiology of BC and related mechanical studies have confirmed the phenomenon and mechanism [ 43 – 46 ]. Our previous study found that the loss of cell polarity has an effect on tumour metastasis in BC [ 47 ], which is consistent with our present results that show that the optimized orthotopic model has a high metastatic rate. Therefore, the orthotopic BC model in our study is theoretically practical to figure out the clinical pathological process in humans.…”

Section: Discussionsupporting

confidence: 93%

Establishment of an optimized orthotopic bladder cancer model in mice

et al. 2022

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Background Bladder cancer (BC) is one of the most common malignancies of the genitourinary system. Animal models offer an important tool to explore tumour initiation, progression, and therapeutic mechanisms. Our aim is to construct an optimized orthotopic BC model which is predictable, reproducible, and convenient. Methods The optimized orthotopic BC model was constructed in male C57BL/6 mice utilizing microsyringes to inoculate them with a murine BC cell line (MB49). Anesthetised mice were inoculated with an MB49 cell suspension (10 µL) at approximately 5 × 106/mL. The whole process of modelling was observed and monitored every 3 days for 21 days utilizing HE staining and transabdominal ultrasonography (TUS). Results In this study, the model showed excellent success rates for tumour formation (96.67%) and metastatic rate (89.66%). Compared to the control group (sham operation), mice in the modelling group had serous cachexia, visible haematuresis and weight loss (all P < 0.05). The lungs, liver, ureter and kidneys were found to have tumour metastasis. Moreover, the average survival time (19.73 ± 1.69 d) of modelling mice was significantly shorter than that of the control mice (P < 0.05), which remained alive. Conclusion Our study established a method using microsyringes to inject murine BC cells into the bladder wall, creating a stable transplantable BC model in mice.

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Section: Discussionsupporting

confidence: 93%

Establishment of an optimized orthotopic bladder cancer model in mice

et al. 2022

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“…[30] Recently, we found that Par3 interacted with ZO-1, a component in tight junctions (TJ), and promoted the metastasis bladder cancer via GSK-3β/Snail/Par3/ZO-1 axis. [31] These results suggest various roles of Par3 in tumor development and further investigations of Par3 regulating the chemosensitivity of breast cancer are warranted.…”

Section: Discussionmentioning

confidence: 92%

Polarity protein Par3 sensitizes breast cancer to paclitaxel by promoting cell cycle arrest

Zhao

Peng

Liang

et al. 2022

Breast Cancer Res Treat

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Purpose Paclitaxel, belongs to tubulin-binding agents (TBAs), showed a great e cacy against breast cancer via stabilizing microtubules. Drug resistance limits its clinical application. Here we aimed to explore a role of Polarity protein Par3 in improving paclitaxel effectiveness.Methods Breast cancer specimens from 45 patients were collected to study the relationship between Par3 expression and paclitaxel e cacy. The Kaplan-Meier method was used for survival analysis. Cell viability was measured in breast cancer cells (SK-BR-3 and T-47D) with Par3 over-expression or knockdown. The ow cytometry assays were performed to measure cell apoptosis and cell cycle. BrdU incorporation assay and Hoechst 33258 staining were performed to measure cell proliferation and cell apoptosis, respectively. Immuno uorescence was used to detect microtubule structures. Results Par3 expression is associated with good response of paclitaxel in breast cancer patients. Consistently, Par3 overexpression signi cantly sensitizes breast cancer cells to paclitaxel by promoting cell apoptosis and reducing cell proliferation. In Par3 overexpressing cells upon paclitaxel treatment, we observed intensi ed cell cycle arrests at metaphase. Further exploration showed that Par3 overexpression stabilizes microtubules of breast cancer cells in response to paclitaxel, and resists to microtubules instability induced by nocodazole, a microtubule-depolymerizing agent. Conclusion Par3 facilitates polymeric forms of tubulin and stabilizes microtubule structure, which aggravates paclitaxel-induced delay at the metaphase-anaphase transition, leading to proliferation inhibition and apoptosis of breast cancer cells. Par3 has a potential role in sensitizing breast cancer cells to paclitaxel, which may provide a more precise assessment of individual treatment and novel therapeutic targets.

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“…We mentioned that Snail is a major regulator of PAR-3 protein expression. Upregulated Snail inhibits PAR-3, then inhibits the localisation of ZO-1 at cell–cell contact points; this is because the ZO-1 protein is likely regulated by the GSK-3β/Snail/Par3/ZO-1 axis [ 78 ].…”

Section: Adherens Junctionsmentioning

confidence: 99%

Role of Cell-Cell Junctions in Oesophageal Squamous Cell Carcinoma

Huang

et al. 2022

Biomolecules

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Cell–cell junctions comprise various structures, including adherens junctions, tight junctions, desmosomes, and gap junctions. They link cells to each other in tissues and regulate tissue homeostasis in critical cellular processes. Recent advances in cell–cell junction research have led to critical discoveries. Cell–cell adhesion components are important for the invasion and metastasis of tumour cells, which are not only related to cell–cell adhesion changes, but they are also involved in critical molecular signal pathways. They are of great significance, especially given that relevant molecular mechanisms are being discovered, there are an increasing number of emerging biomarkers, targeted therapies are becoming a future therapeutic concern, and there is an increased number of therapeutic agents undergoing clinical trials. Oesophageal squamous cell carcinoma (ESCC), the most common histological subtype of oesophageal cancer, is one of the most common cancers to affect epithelial tissue. ESCC progression is accompanied by the abnormal expression or localisation of components at cell–cell junctions. This review will discuss the recent scientific developments related to the molecules at cell–cell junctions and their role in ESCC to offer valuable insights for readers, provide a global view of the relationships between position, construction, and function, and give a reference for future mechanistic studies, diagnoses, and therapeutic developments.

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Loss of polarity protein Par3, via transcription factor Snail, promotes bladder cancer metastasis

Cited by 11 publications

References 39 publications

Establishment of an optimized orthotopic bladder cancer model in mice

Establishment of an optimized orthotopic bladder cancer model in mice

Polarity protein Par3 sensitizes breast cancer to paclitaxel by promoting cell cycle arrest

Role of Cell-Cell Junctions in Oesophageal Squamous Cell Carcinoma

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