Long non‑coding RNA MALAT1 correlates with cell viability and mobility by targeting miR‑22‑3p in renal cell carcinoma via the PI3K/Akt pathway

Zhong, Li; Ma, Zhiqiang; Xu, Xiangdong

doi:10.3892/or.2018.6853

Cited by 16 publications

(16 citation statements)

References 38 publications

(46 reference statements)

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“…To a further extent, PI3K/AKT/mTOR is identified as a highly enriched pathway in translocation RCC with TFE3 fusion (TFE3-tRCC) by miRNA microarray analysis [258]. Besides that PIK3R1 regulates EMT and stem-like phenotype of RCC cells through the AKT/GSK3β/CTNNB1 pathway [259], FoxO, PKCε, TPD52, NOTCH1, ETS2, miR-19b, -122, -182, -193a-3p, -195, and -224, as well as LncRNA MALAT1, TP73-AS1 and HOTTIP modulate proliferation, apoptosis, invasion, metastasis, or EMT via PI3K/ AKT pathway [260][261][262][263][264][265][266][267][268][269][270][271][272]. However, only a few of clinical trials of PI3K/AKT inhibitors in touch try to offer hope for KC patients (Tables 2 and 3).…”

Section: Dysregulation Of the Pi3k/akt Pathway In The Genitourinary Smentioning

confidence: 99%

Role of PI3K/AKT pathway in cancer: the framework of malignant behavior

et al. 2020

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Given that the PI3K/AKT pathway has manifested its compelling influence on multiple cellular process, we further review the roles of hyperactivation of PI3K/AKT pathway in various human cancers. We state the abnormalities of PI3K/AKT pathway in different cancers, which are closely related with tumorigenesis, proliferation, growth, apoptosis, invasion, metastasis, epithelial-mesenchymal transition, stem-like phenotype, immune microenvironment and drug resistance of cancer cells. In addition, we investigated the current clinical trials of inhibitors against PI3K/AKT pathway in cancers and found that the clinical efficacy of these inhibitors as monotherapy has so far been limited despite of the promising preclinical activity, which means combinations of targeted therapy may achieve better efficacies in cancers. In short, we hope to feature PI3K/ AKT pathway in cancers to the clinic and bring the new promising to patients for targeted therapies.

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Section: Dysregulation Of the Pi3k/akt Pathway In The Genitourinary Smentioning

confidence: 99%

Role of PI3K/AKT pathway in cancer: the framework of malignant behavior

et al. 2020

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“…22 Li et al proved that MALAT1 influences the proliferation and migration of renal cell carcinoma cells by targeting miR-22-3p. 23 However, whether the regulatory role of MALAT1 on GC is associated with miR-22 remains unclear.…”

Section: Introductionmentioning

confidence: 99%

<p>Silencing of LncRNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 Inhibits the Proliferation and Promotes the Apoptosis of Gastric Cancer Cells Through Regulating microRNA-22-3p-Mediated ErbB3</p>

Zhao

Zhang

et al. 2020

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Purpose: This study aimed to investigate the regulatory effects and mechanisms of long non-coding RNA (LncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on gastric cancer (GC) cells. Methods: The expression of MALAT1 was detected in GC tissues and two GC cell lines (SGC-7901 and BGC-823). MALAT1 was overexpressed and silenced in GC cells by the transfection of pcDNA-MALAT1 and siRNA-MALAT1, respectively. The proliferation and apoptosis of transfected cells, as well as the tumor volume and weight in mice injected with transfected cells were determined. After identifying the interaction between microRNA-22-3p (miR-22-3p) and MALAT1/epidermal growth factor receptor 3 (ErbB3), the effects of miR-22-3p/ErbB3 silencing on the proliferation and apoptosis of GC cells were evaluated. Results: MALAT1 was significantly upregulated in GC tissues and cells and negatively associated with the survival of GC patients. Overexpression of MALAT1 significantly promoted the proliferation and inhibited the apoptosis of SGC-7901 cells, while silencing of MALAT1 exerts contrary effects on BGC-823 cells. Silencing of MALAT1 also significantly inhibited the tumor growth in mice. In addition, MALAT1 negatively regulated its target miR-22-3p. Silencing of miR-22-3p reversed the anti-tumor effects of MALAT1 silencing on GC cells. MiR-22-3p negatively regulated its target ErbB3. Silencing of ErbB3 reversed the tumor-promoting effects of miR-22-3p silencing on GC cells. Conclusion: Silencing of MALAT1 inhibited the proliferation and promoted the apoptosis of GC cells through upregulating miR-22-3p and downregulating ErbB3.

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“…44,45 For example, the lncRNA metastasis Associated Lung Adenocarcinoma Transcript 1 is associated with proliferation and migration in RCC and targeting this lncRNA with short hairpin RNA reduced these activities. 46 A more comprehensive exploration of microRNAs and lncRNA in cancer can be found in recent cancer studies. 44,45,47 A wide range of options exist to target these biomolecules.…”

Section: Biologicsmentioning

confidence: 99%

Potential New Therapeutic Approaches for Renal Cell Carcinoma

Yang

Chen

2020

Seminars in Nephrology

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Renal cell carcinoma (RCC) is increasing in incidence and one third of newly diagnosed cases already are metastatic. The metastatic spread of solid tumors renders RCC incurable by surgical resection and consequently more difficult to treat. New molecular-targeted therapies have played a pivotal role in RCC treatment. Unfortunately, tumors frequently develop resistance to these targeted therapies by activating bypass pathways in which alternative signaling or biochemical pathways are activated in response to targeted inhibition of a signaling pathway, allowing cancer cells to continue to survive. Although the advent of immunotherapy with checkpoint inhibitors has led to significant changes in the treatment landscape for advanced RCC, many issues remain to be resolved. For these reasons, there is an urgent need to develop novel therapies and new treatment paradigms for patients with RCC. Much research has been performed thus far in identifying novel targets and treatment strategies in RCC and many of these currently are under investigation and/or in clinical trials. In this article, we discuss therapeutic options in the management of RCC with a focus on the new therapeutic approaches currently investigated in research and for use in the clinic. We divide these potential novel therapies into five groups: nonbiologics, small-molecule drugs, biologics, immunomodulatory therapies, and peptide drugs. We also present some therapeutics and treatment paradigms.

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Long non‑coding RNA MALAT1 correlates with cell viability and mobility by targeting miR‑22‑3p in renal cell carcinoma via the PI3K/Akt pathway

Cited by 16 publications

References 38 publications

Role of PI3K/AKT pathway in cancer: the framework of malignant behavior

Role of PI3K/AKT pathway in cancer: the framework of malignant behavior

<p>Silencing of LncRNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 Inhibits the Proliferation and Promotes the Apoptosis of Gastric Cancer Cells Through Regulating microRNA-22-3p-Mediated ErbB3</p>

Potential New Therapeutic Approaches for Renal Cell Carcinoma

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