Tumor Suppressor in Lung Cancer-1 Is a Prognostic Predictor for the Recurrence and Progression of Non-Muscle-Invasive Bladder Cancer

Chen, Yegang; Yang, Yongjiao; Liu, Li; Wang, Shangren; Song, Hong Suk; Liu, Xiaoqiang

doi:10.1159/000438492

Cited by 4 publications

(2 citation statements)

References 28 publications

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“…Based on the clinicopathological manifestations described above, CADM1 can be utilized as a more practical clinical biomarker (Lee et al, 2013;Chen et al, 2016). The specific reason is that CADM1 is downregulated in most cases due to its promoter methylation as well as being related to the progression of malignant tumors, advanced classification, poor 5-year survival, and high recurrence rate; for example, in cervical cancer, CADM1 can be used as a biomarker to participate in the assessment of cervical epithelial lesions (Del Pino et al, 2019;El Aliani et al, 2021).…”

Section: Cadm1 As a Biomarker For Cancer Diagnosis And Prognosismentioning

confidence: 99%

Functional and Clinical Characteristics of Cell Adhesion Molecule CADM1 in Cancer

Gao

Zhang

2021

Front. Cell Dev. Biol.

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The cell adhesion molecule CADM1, which participates in cell adhesion and signal transduction, has a regulatory effect on the development of tumors. CADM1 is often involved in malignant tumors of multiple organ systems, such as the respiratory and digestive systems. Upregulated CADM1 promotes tumor cell apoptosis and inhibits malignant proliferation. Along with cell cycle-related proteins, it participates in regulating signaling pathways, such as EMT, STAT3, and AKT, and plays an important role in inhibiting invasion and migration. Considering clinical characteristics, low CADM1 expression is associated with aggressive tumors and poor prognosis. In addition, some long non-coding RNAs (lncRNAs) or miRNAs directly or indirectly act on CADM1 to regulate tumor growth and motility. Interestingly, CADM1 function differs in adult T-cell leukemia/lymphoma (ATLL), and NF-κB is thought to be involved in this process. Taken together, CADM1 could be a potential biomarker for early diagnosis and a target for cancer treatment in future clinical practices.

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Section: Cadm1 As a Biomarker For Cancer Diagnosis And Prognosismentioning

confidence: 99%

Functional and Clinical Characteristics of Cell Adhesion Molecule CADM1 in Cancer

Gao

Zhang

2021

Front. Cell Dev. Biol.

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“…Bladder cancer ranks 13th in the causes for cancer-associated mortality worldwide and is the most common type of urological cancer in China (1). Muscle-invasive bladder cancer constitutes ~30% of newly diagnosed cases of bladder cancer (2).…”

Section: Introductionmentioning

confidence: 99%

Role of 5‑Aza‑CdR in mitomycin‑C chemosensitivity of T24 bladder cancer cells

et al. 2017

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Abstract. Chemotherapeutic insensitivity is one of key obstacles to effectively treating muscle invasive bladder cancer. 5-Aza-2'-deoxycytidine (5-Aza-CdR) has been identified as a tumor suppressive agent in various types of cancer. The aim of the present study was to identify the effects of 5-Aza-CdR on the mitomycin-C (MMC) chemosensitivity of T24 bladder cancer cells and investigate the underlying mechanisms. T24 cells were treated with a combination of MMC and 5-Aza-CdR at various concentrations. The rates of proliferation and apoptosis were assessed by an MTT assay and flow cytometry, respectively. The expression of drug resistance-associated proteins, including P-glycoprotein (P-gp) and multidrug resistance-associated protein 1 (MRP1), and autophagy-associated proteins, including beclin 1, nucleoporin 62 (p62) and autophagy protein 5 (ATG5) were detected with western blotting. Treatment with 5-Aza-CdR significantly promoted the MMC chemosensitivity of T24 cells. The proliferation of T24 cells was significantly inhibited with increasing 5-Aza-CdR concentration, whereas apoptosis was significantly increased. This was associated with the decreased expression of P-gp, MRP1, beclin 1, p62 and ATG5. In conclusion, 5-Aza-CdR enhanced MMC chemosensitivity in bladder cancer T24 cells, which may be caused by the suppression of drug resistance-and autophagy-associated proteins.

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Folic acid inhibits nasopharyngeal cancer cell proliferation and invasion via activation of FRα/ERK1/2/TSLC1 pathway

Zhi-biao

Jin

et al. 2017

Bioscience Reports

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Folic acid (FA), which is necessary for normal cell division of mammals, has been implicated to be involved in many tumors. Dietary FA intake has been reported to be associated with a lower risk of nasopharyngeal cancer (NPC). However, the molecular mechanisms of FA in NPC cells remain unclear. In the present study, we found that FA treatment dose dependently inhibited the proliferation, invasion and migration of NPC cells, via folate receptor α (FRα). We further found that FA, bound to FRα, induced the activation of MEK/ERK1/2, and increased the expressions of TSLC1 and E-cadherin. Moreover, blocking of ERK1/2 activation attenuated FA-mediated increase in TSLC1 expression. In addition, knockdown of TSLC1 abolished the FA-mediated inhibition of cell proliferation, invasion and migration, and suppressed the FA-mediated increase oinE-cadherin expression in NPC cells. Taken together, our data suggest that FA treatment inhibits NPC cell proliferation and invasion via activation of FRα/ERK1/2/ TSLC1 signaling pathway. Therefore, FA could be explored as a therapeutic drug for the treatment of NPC, and TSLC1 may act as a tumor suppressor in NPC.

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Tumor Suppressor in Lung Cancer-1 Is a Prognostic Predictor for the Recurrence and Progression of Non-Muscle-Invasive Bladder Cancer

Cited by 4 publications

References 28 publications

Functional and Clinical Characteristics of Cell Adhesion Molecule CADM1 in Cancer

Functional and Clinical Characteristics of Cell Adhesion Molecule CADM1 in Cancer

Role of 5‑Aza‑CdR in mitomycin‑C chemosensitivity of T24 bladder cancer cells

Folic acid inhibits nasopharyngeal cancer cell proliferation and invasion via activation of FRα/ERK1/2/TSLC1 pathway

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