Long non-coding RNAs as new players in bladder cancer: Lessons from pre-clinical and clinical studies

Mirzaei, Sepideh; Paskeh, Mahshid Deldar Abad; Hashemi, Farid; Zabolian, Amirhossein; Hashemi, Mehrdad; Entezari, Maliheh; Tabari, Teimour; Ashrafizadeh, Milad; Raee, Pourya; Aghamiri, Seyed Mahmoud Reza; Aref, Amir Reza; Leong, Hin Chong; Kumar, Alan Prem; Samarghandian, Saeed; Zarrabi, Ali; Hushmandi, Kiavash

doi:10.1016/j.lfs.2021.119948

Cited by 31 publications

(21 citation statements)

References 238 publications

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“…For example, NETs can promote bladder cancer resist to radiotherapy (Wu et al, 2018); MMP-9 is significantly expressed in high-grade bladder cancer compare with that in low-grade ones (Shinde-Jadhav et al, 2021). The high expression of MMP-9 can promote the metastasis of bladder cancer has been confirmed, and there is evidence that the process is associated with MMP-9 promoted epithelial-mesenchymal transition (EMT) in bladder cancer (Ashrafizadeh et al, 2020a;Mirzaei et al, 2021a;Mirzaei et al, 2021b). NE can promote the proliferation and invasion of bladder cancer and other malignant behaviors in vitro (Yang and Sun, 2004).…”

Section: Rcds In Bladder Malignanciesmentioning

confidence: 98%

Regulated Cell Death in Urinary Malignancies

Nie

Chen

Gao

et al. 2021

Front. Cell Dev. Biol.

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Urinary malignancies refer to a series of malignant tumors that occur in the urinary system and mainly include kidney, bladder, and prostate cancers. Although local or systemic radiotherapy and chemotherapy, immunotherapy, castration therapy and other methods have been applied to treat these diseases, their high recurrence and metastasis rate remain problems for patients. With in-depth research on the pathogenesis of urinary malignant tumors, this work suggests that regulatory cell death (RCD) plays an important role in their occurrence and development. These RCD pathways are stimulated by various internal and external environmental factors and can induce cell death or permit cell survival under the control of various signal molecules, thereby affecting tumor progression or therapeutic efficacy. Among the previously reported RCD methods, necroptosis, pyroptosis, ferroptosis, and neutrophil extracellular traps (NETs) have attracted research attention. These modes transmit death signals through signal molecules, such as cysteine-aspartic proteases (caspase) family and tumor necrosis factor-α (TNF-α) that have a wide and profound influence on tumor proliferation or death and even change the sensitivity of tumor cells to therapy. This review discussed the effects of necroptosis, pyroptosis, ferroptosis, and NETs on kidney, bladder and prostate cancer and summarized the latest research and achievements in these fields. Future directions and possibility of improving the denouement of urinary system tumors treatment by targeting RCD therapy were also explored.

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Section: Rcds In Bladder Malignanciesmentioning

confidence: 98%

Regulated Cell Death in Urinary Malignancies

Nie

Chen

Gao

et al. 2021

Front. Cell Dev. Biol.

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“…Our results indicated that linc02470 is a potent ceRNA competitor of miR-143-3p, although other ceRNA competitors of miR-143 or miR-145 still need to be explored in the future. Dysregulation of the EMT process has become a major issue in bladder cancer progression and therapeutic responses [ 10 , 11 ], and lncRNAs or other ncRNAs participate in important regulatory processes (reviewed in [ 14 , 15 , 16 , 17 ]). The ceRNA hypothesis has been employed as an easily accessible strategy to discover interactions between EMT members and lncRNAs or other ncRNAs [ 12 ].…”

Section: Discussionmentioning

confidence: 99%

“…Long noncoding RNAs (lncRNA) are noncoding RNAs with lengths exceeding 200 nt that are involved in a variety of cellular physiological processes [ 13 ] and participate in bladder cancer initiation, progression, and therapeutic resistance (reviewed in [ 14 , 15 , 16 , 17 ]). In addition, microRNAs (miRNAs) function as ubiquitous posttranscriptional regulators that affect RNA stability and translational rate by pairing to miRNA response elements within target RNAs [ 18 , 19 ].…”

Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA LINC02470 Sponges MicroRNA-143-3p and Enhances SMAD3-Mediated Epithelial-to-Mesenchymal Transition to Promote the Aggressive Properties of Bladder Cancer

Huang

Tsai

et al. 2022

Cancers

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Bladder cancer progression and metastasis have become major threats in clinical practice, increasing mortality and therapeutic refractoriness; recently, epigenetic dysregulation of epithelial-to-mesenchymal transition (EMT)-related signaling pathways has been explored. However, research in the fields of long noncoding RNA (lncRNA) and competing endogenous RNA (ceRNA) regulation in bladder cancer progression is just beginning. This study was designed to determine potential EMT-related ceRNA regulation in bladder cancer progression and elucidate the underlying mechanisms that provoke aggressiveness. After screening the intersection of bioinformatic pipelines, LINC02470 was identified as the most upregulated lncRNA during bladder cancer initiation and progression. Both in vitro and in vivo biological effects indicated that LINC02470 promotes bladder cancer cell viability, migration, invasion, and tumorigenicity. On a molecular level, miR-143-3p directly targets and reduces both LINC02470 and SMAD3 RNA expression. Therefore, the LINC02470–miR-143-3p–SMAD3 ceRNA axis rescues SMAD3 translation upon LINC02470 sponging miR-143-3p, and SMAD3 consequently activates the TGF-β-induced EMT process. In conclusion, this is the first study to demonstrate that LINC02470 plays a pivotally regulatory role in the promotion of TGF-β-induced EMT through the miR-143-3p/SMAD3 axis, thereby aggravating bladder cancer progression. Our study warrants further investigation of LINC02470 as an indicatively prognostic marker of bladder cancer.

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“…3,4 Currently, BC treatment is still based on surgical resection, accompanied by bladder perfusion chemotherapy, systemic chemotherapy, and radiotherapy. [5][6][7][8] Although emerging targeted therapies and immunotherapy provide new treatments for BC, the high recurrence rate still leads to poor treatment effects for BC. 9 Therefore, exploring new pathogenic genes will help us gain greater insight into the mechanism of BC occurrence and development, and will contribute to the development of effective molecular markers for early diagnosis, detection of metastasis, and recurrence of BC, and will identify potential BC treatment targets.…”

Section: Introductionmentioning

confidence: 99%

KLF16 Downregulates the Expression of Tumor Suppressor Gene TGFBR3 to Promote Bladder Cancer Proliferation and Migration

Chen

Wang²,

et al. 2022

CMAR

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Krüppel-like factors (KLFs), which comprise 17 family members, exert important functions during the development of cancer. The role of KLF16 seems controversial in carcinogenesis because both tumor suppressive and promoting effects have been reported. Methods:The expression level of KLF16 was analyzed based on public data sets from The Cancer Genome Atlas (TCGA) and evaluated by immunohistochemical (IHC) staining. CCK8 assay, colony formation analysis, transwell assays and the PI/Annexin V-APC assay kit were performed to detect cell growth, colony formation, cell migration and apoptosis of BC cells. Xenograft tumorigenesis assay was performed to detect the KLF16 expression on BC growth in vivo. Dual-luciferase reporter assay and chromatin immunoprecipitation (ChIP)-qPCR assay were performed to analyze the interaction between KLF16 and its target. Results: In this study, we explored the role of KLF16 in bladder cancer (BC). We demonstrated that KLF16 was overexpressed in human BC tissues. The high expression of KLF16 was a potential predictor of a poor prognosis in patients with BC. Interference with KLF16 expression in 563 cells, having relatively higher levels of KLF16, repressed cell proliferation and migration. In contrast, upregulation of KLF16 in T24 cells enhanced cellular function, including cell growth and migration. KLF16 also suppressed the apoptosis of BC cells. Additionally, KLF16 inhibited the expression of the TGF-type III receptor (TGFBR3) by binding to its promoter sequence and reducing transcriptional activity. There was a negative correlation between KLF16 and TGFBR3 in human BC tissues. Furthermore, TGFBR3 was revealed to be a negative regulator of BC cell proliferation and migration. KLF16 also supported BC tumorigenesis by downregulating TGFBR3 expression in vivo. Discussion: These results suggested that KLF16 acts as an oncogene in BC through transcriptional inactivation of TGFBR3. This study provides evidence that targeting the KLF16/TGFBR3 axis may be beneficial for BC patients.

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Long non-coding RNAs as new players in bladder cancer: Lessons from pre-clinical and clinical studies

Cited by 31 publications

References 238 publications

Regulated Cell Death in Urinary Malignancies

Regulated Cell Death in Urinary Malignancies

Long Noncoding RNA LINC02470 Sponges MicroRNA-143-3p and Enhances SMAD3-Mediated Epithelial-to-Mesenchymal Transition to Promote the Aggressive Properties of Bladder Cancer

KLF16 Downregulates the Expression of Tumor Suppressor Gene TGFBR3 to Promote Bladder Cancer Proliferation and Migration

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