LncRNA FENDRR Upregulation Promotes Hepatic Carcinoma Cells Apoptosis by Targeting miR-362-5p Via NPR3 and p38-MAPK Pathway

Qian, Guang-yu; Jin, Xiaoyan; Zhang, Louwei

doi:10.1089/cbr.2019.3468

Cited by 20 publications

(16 citation statements)

References 31 publications

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“…Similarly, Zhang et al have validated that GAS5 expression was reduced in papillary TC tissues and cells, 22 and this downregulation of GAS5 in TC has been elucidated by Guo et al as well 8 . Moreover, it has been demonstrated that miR‐362‐5p expression was elevated in bladder cancer tissues, 23 and it has been verified that miR‐362‐5p was upregulated in hepatic carcinoma tissues and cells 24 . As for SMG1, Yin et al have found the downregulation of SMG1 in hepatocellular carcinoma (HCC), 25 and it was also identified that SMG1 was downregulated in patients with acute myeloid leukemia (AML) 26 .…”

Section: Discussionmentioning

confidence: 74%

“…Literature has indicated that the suppressive role of lncRNA FENDRR overexpression in HCC cell growth was reversed by miR-362-5p. 24 It has also been demonstrated that miR-192 and miR-215 inhibition suppressed gastric cancer cell growth, while these effects were reversed by SMG1 silencing. 30 All of these data are helpful for exploring the molecular mechanisms of TC.…”

Section: Discussionmentioning

confidence: 98%

“…8 Moreover, it has been demonstrated that miR-362-5p expression was elevated in bladder cancer tissues, 23 and it has been verified that miR-362-5p was upregulated in hepatic carcinoma tissues and cells. 24 As for SMG1, Yin et al have found the downregulation of SMG1 in hepatocellular carcinoma (HCC), 25 and it was also identified that SMG1 was downregulated in patients with acute myeloid leukemia (AML). 26 In addition, the Akt/mTOR pathway has been uncovered to be activated in cervical cancer.…”

Section: Discussionmentioning

confidence: 99%

“…Rescue experiments were performed in our research and we found that miR‐362‐5p mimic reversed the effect of GAS5 overexpression on 131 I‐resistant TC cells, and the effect of miR‐362‐5p mimic on 131 I‐resistant TC cells could be abrogated by SMG1 upregulation. Literature has indicated that the suppressive role of lncRNA FENDRR overexpression in HCC cell growth was reversed by miR‐362‐5p 24 . It has also been demonstrated that miR‐192 and miR‐215 inhibition suppressed gastric cancer cell growth, while these effects were reversed by SMG1 silencing 30 .…”

Section: Discussionmentioning

confidence: 99%

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LncRNA GAS5 sponges miR‐362‐5p to promote sensitivity of thyroid cancer cells to ¹³¹I by upregulating SMG1

Lin

et al. 2020

IUBMB Life

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This study aims to investigate the role of lncRNA growth arrest-specific transcript 5 (GAS5)/miR-362-5p/suppressor of morphogenesis in the genitalia 1 (SMG1) axis in 131 I-resistance in thyroid cancer (TC). GAS5, miR-362-5p, and SMG1 expression in TC tissues was assessed and the 131 I-resistant TC cells were established, which were treated with altered GAS5, miR-362-5p, and SMG1. The proliferation and apoptosis of 131 I-resistant TC cells were detected, and the expression of Akt/mTOR signaling pathway-related proteins was assessed. Binding relations between GAS5 and miR-362-5p, and miR-362-5p and SMG1 were confirmed. The role of GAS5 in 131 I-resistant TC cell growth in vivo was observed. GAS5 was downregulated and miR-362-5p was upregulated in TC tissues and 131 I-resistant cells. The 131 I-resistant TC cells had enhanced proliferation and repressed apoptosis, and the Akt/mTOR signaling pathway was activated. Overexpressed GAS5 strengthened 131 I sensitivity and suppressed TC cell growth, while upregulated miR-362-5p had an opposite effect. MiR-362-5p upregulation reversed the effect of GAS5, and SMG1 overexpression eliminated the impact of miR-362-5p upregulation on 131 I-resistant TC cells. GAS5 competitively binds to miR-362-5p and SMG1 is targeted by miR-362-5p. GAS5 sponges miR-362-5p to promote sensitivity of TC cells to 131 I by upregulating SMG1 and inactivating Akt/mTOR signaling pathway.

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Section: Discussionmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

LncRNA GAS5 sponges miR‐362‐5p to promote sensitivity of thyroid cancer cells to ¹³¹I by upregulating SMG1

Lin

et al. 2020

IUBMB Life

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“…Li et al reported that MRCCAT1 promotes metastasis of clear cell renal cell carcinoma via inhibiting NPR3 expression [34]. However, in hepatocellular carcinoma, FENDRR promoted cancer cells apoptosis by targeting miR-362-5p via stimulating NPR3 expression [35]. In addition, NPR3 upregulation could also promotes the proliferation of colorectal cancer cells [36].…”

Section: Discussionmentioning

confidence: 99%

A signature of seven immune-related genes predicts overall survival in male gastric cancer patients

Wang

et al. 2020

Preprint

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Background: Gastric cancer (GC) is one of the most fatal malignant tumors with a high mortality rate. Male sex has been proven as an independent risk factor for GC. This study aimed to identify immune-related genes (IRGs) for the prognosis of male GC.Method: RNA sequencing and clinical data were obtained from The Cancer Genome Atlas (TCGA) database. Differentially expressed IRGs between male GC and normal tissues were identified by integrated bioinformatics analysis. Univariate and multivariate Cox regression analysis were applied to screen survival-associated IRGs. Then, GC patients were separated into high- and low-risk groups based on the median risk score. Furthermore, a nomogram was constructed based on the TCGA dataset. The prognostic value of the risk signature model was evaluated by Kaplan-Meier curve, receiver operating characteristic (ROC), Harrell’s concordance index and calibration curves. In addition, the gene expression dataset from Gene Expression Omnibus (GEO) was also downloaded for external validation. The relative proportions of 22 types of infiltrating immune cells in each male GC sample were evaluated using CIBERSORT.Results: A total of 276 differentially expressed IRGs were screened, including 189 up-regulated and 87 down-regulated genes. Subsequently, a seven-IRGs signature (LCN12, CCL21, RNASE2, CGB5, NRG4, AGTR1 and NPR3) was identified and showed a significant association with the overall survival (OS) of male GC patients. Survival analysis indicated that patients with high-risk group exhibited a poor clinical outcome. The result of multivariate analysis revealed that the risk score was an independent prognostic factor. The established nomogram could be used to evaluate the prognosis of individual male GC patients. Further analysis showed that the prognostic model had an excellent predictive performance in both TCGA and validated cohorts. Besides, the result of tumor-infiltrating immune cell analysis indicated that the seven-IRGs signature could reflect the status of the tumor immune microenvironment.Conclusions: Our study developed a novel seven-IRGs risk signature for individualized survival prediction of male GC patients.

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Converting “cold” to “hot”: epigenetics strategies to improve immune therapy effect by regulating tumor‐associated immune suppressive cells

Tang,

Cui,

Liu

et al. 2024

Cancer Communications

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Significant developments in cancer treatment have been made since the advent of immune therapies. However, there are still some patients with malignant tumors who do not benefit from immunotherapy. Tumors without immunogenicity are called “cold” tumors which are unresponsive to immunotherapy, and the opposite are “hot” tumors. Immune suppressive cells (ISCs) refer to cells which can inhibit the immune response such as tumor‐associated macrophages (TAMs), myeloid‐derived suppressor cells (MDSCs), regulatory T (Treg) cells and so on. The more ISCs infiltrated, the weaker the immunogenicity of the tumor, showing the characteristics of “cold” tumor. The dysfunction of ISCs in the tumor microenvironment (TME) may play essential roles in insensitive therapeutic reaction. Previous studies have found that epigenetic mechanisms play an important role in the regulation of ISCs. Regulating ISCs may be a new approach to transforming “cold” tumors into “hot” tumors. Here, we focused on the function of ISCs in the TME and discussed how epigenetics is involved in regulating ISCs. In addition, we summarized the mechanisms by which the epigenetic drugs convert immunotherapy‐insensitive tumors into immunotherapy‐sensitive tumors which would be an innovative tendency for future immunotherapy in “cold” tumor.

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LncRNA FENDRR Upregulation Promotes Hepatic Carcinoma Cells Apoptosis by Targeting miR-362-5p Via NPR3 and p38-MAPK Pathway

Cited by 20 publications

References 31 publications

LncRNA GAS5 sponges miR‐362‐5p to promote sensitivity of thyroid cancer cells to ¹³¹I by upregulating SMG1

LncRNA GAS5 sponges miR‐362‐5p to promote sensitivity of thyroid cancer cells to ¹³¹I by upregulating SMG1

A signature of seven immune-related genes predicts overall survival in male gastric cancer patients

Converting “cold” to “hot”: epigenetics strategies to improve immune therapy effect by regulating tumor‐associated immune suppressive cells

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LncRNA FENDRR Upregulation Promotes Hepatic Carcinoma Cells Apoptosis by Targeting miR-362-5p Via NPR3 and p38-MAPK Pathway

Cited by 20 publications

References 31 publications

LncRNA GAS5 sponges miR‐362‐5p to promote sensitivity of thyroid cancer cells to 131I by upregulating SMG1

LncRNA GAS5 sponges miR‐362‐5p to promote sensitivity of thyroid cancer cells to 131I by upregulating SMG1

A signature of seven immune-related genes predicts overall survival in male gastric cancer patients

Converting “cold” to “hot”: epigenetics strategies to improve immune therapy effect by regulating tumor‐associated immune suppressive cells

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LncRNA GAS5 sponges miR‐362‐5p to promote sensitivity of thyroid cancer cells to ¹³¹I by upregulating SMG1

LncRNA GAS5 sponges miR‐362‐5p to promote sensitivity of thyroid cancer cells to ¹³¹I by upregulating SMG1