High expression of hnRNPA1 promotes cell invasion by inducing EMT in gastric cancer

Chen, Yahua; Li, Jun; Wang, Wei; Li, Xiang; Wang, Jide; Liu, Side; Zhou, Haoming; Guo, Zheng

doi:10.3892/or.2018.6273

Cited by 44 publications

(46 citation statements)

References 32 publications

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“…The hnRNPA1 protein was a molecule target of Que in PC-3 cells, 29 and overexpression of hnRNPA1 was related to cancer cell epithelial-to-mesenchymal transition (EMT), which was considered to be a mechanism of cancer cell migration. 30,31 Therefore, hnRNPA1 may be related to cell migration and metastasis, quercetin could decrease the hnRNPA1 expression to inhibit EMT of cancer cell. In this study, transwell assays revealed that Que combined with PTX effectively inhibited cell migration.…”

Section: Discussionmentioning

confidence: 99%

<p>Quercetin Enhanced Paclitaxel Therapeutic Effects Towards PC-3 Prostate Cancer Through ER Stress Induction and ROS Production</p>

Zhang

Huang

et al. 2020

OTT

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Introduction: Prostate cancer is one of the most common cancers threatening public health worldwide. Although chemotherapy plays an important role in treating prostate cancer, it leads to many adverse effects and is prone to drug resistance. Quercetin, a natural product, is used in traditional Chinese medicine because of its strong antitumor activity and few side effects. Methods: In this study, we combined quercetin and paclitaxel to kill prostate cancer cells in vivo and in vitro, and we investigated the relevant mechanism of this combination treatment. After the cancer cells were treated with quercetin or/and paclitaxel, cell growth inhibition, apoptosis, the cell cycle, reactive oxygen species (ROS) generation, and several endoplasmic reticulum (ER) stress signaling pathway related gene expressions were evaluated. Results: The combined treatment with quercetin and paclitaxel significantly inhibited cell proliferation, increased apoptosis, arrested the cell cycle at the G2/M phase, inhibited cell migration, dramatically induced ER stress to occur, and increased ROS generation. In a PC-3 cancer-bearing murine model, this combination treatment exerted the most beneficial therapeutic effects, and quercetin increased the cancer cell-killing effects of paclitaxel, with nearly no side effects compared with the single paclitaxel treatment group. Conclusion: Combination treatment possessed enhanced anti-cancer effects, and these results will provide a basis for treating prostate cancer using a combination of quercetin and paclitaxel.

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Section: Discussionmentioning

confidence: 99%

<p>Quercetin Enhanced Paclitaxel Therapeutic Effects Towards PC-3 Prostate Cancer Through ER Stress Induction and ROS Production</p>

Zhang

Huang

et al. 2020

OTT

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“…Therefore, investigation of the molecular mechanism of NSCLC metastasis is urgent. Epithelial‐mesenchymal transition (EMT) has been demonstrated to be an crucial process for the migration, invasion, and metastasis of cancer cell (Chen et al, ). Hence, inhibiting EMT process could be helpful to suppress the metastasis of NSCLC cell and prolong the survival time of patients with NSCLC.…”

Section: Introductionmentioning

confidence: 99%

LncRNA MAFG‐AS1 facilitates the migration and invasion of NSCLC cell via sponging miR‐339‐5p from MMP15

Jia

Wang

Liu³

et al. 2019

Cell Biology International

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Non-small-cell carcinoma (NSCLC) is the most common cancer along with high mortality rate worldwide. In the present study, our data showed that lncRNA MAF BZIP Transcription Factor G Antisense RNA 1 (MAFG-AS1) was over-expressed in NSCLC tissues and cell lines. Overexpression of MAFG-AS1 promoted the migration, invasion and enhanced epithelialmesenchymal transition (EMT) of NSCLC cell. In addition, miR-339-5p was predicted to be a target of MAFG-AS1 and the level of miR-339-5p was down-regulated in NSCLC. Over-expression of MAFG-AS1 significantly decreased the level of miR-339-5p in NSCLC cell. Moreover, the matrix metalloproteinase 15 (MMP15) was identified to be a target of miR-339-5p. The level of MMP15 was negatively regulated by miR-339-5p whereas positively controlled by MAFG-AS1. In addition, up-regulation of miR-339-5p neutralized the promoting impact of MAFG-AS1 on the migration, invasion and EMT of NSCLC cell. Finally, the xenograft model suggested that MAFG-AS1 promoted the metastasis of NSCLC cell in vivo. Altogether, we proved that MAFG-AS1-miR-339-5p-MMP15 axis might be a promising therapeutic target for the treatment of patients with NSCLC.

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“…29 A previous study demonstrated that HNRNPA1 promoted cell invasion in GC by inducing epithelial-to-mesenchymal transition. 30 In the current study, we revealed that knockdown HNRNPA1 could also inhibit cell proliferation, migration, and invasion while promote cell apoptosis in GC cell lines. Intriguingly, inhibition of miR-339 or overexpression of HNRNPA1 abrogated the regulatory effect of RP11-81H3.2 knockdown, which indicates the interaction axis among RP11-81H3.2-miR-339-HNRNPA1.…”

Section: Discussionmentioning

confidence: 56%

RP11‐81H3.2 promotes gastric cancer progression through miR‐339‐HNRNPA1 interaction network

et al. 2020

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Recent studies have demonstrated that various long non‐coding RNAs (lncRNAs) participate in the gastric cancer (GC) development and metastasis. Some lncRNAs exert their regulatory function by interacting with microRNAs. Here we identified a novel lncRNA RP11‐81H3.2 that was highly expressed in the GC tissue and cell lines. RP11‐81H3.2 knockdown significantly inhibited the proliferation, migration, and invasion of GC cells. Mechanistically, we demonstrated that RP11‐81H3.2 directly interacted with miR‐339 while miR‐339 regulated the HNRNPA1 expression by targeting HRRNPA1 3’‐UTR. RP11‐81H3.2‐miR‐339‐HNRNPA1 interaction network regulated the GC cell proliferation, migration, and invasion. Moreover, our results confirmed that RP11‐81H3.2 knockdown suppressed the tumor growth of GC in a xenograft model in vivo. In summary, the results suggest that RP11‐81H3.2 functions as an oncogene in GC and could be utilized as a promising diagnosis and therapeutic marker for GC treatment.

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High expression of hnRNPA1 promotes cell invasion by inducing EMT in gastric cancer

Cited by 44 publications

References 32 publications

<p>Quercetin Enhanced Paclitaxel Therapeutic Effects Towards PC-3 Prostate Cancer Through ER Stress Induction and ROS Production</p>

<p>Quercetin Enhanced Paclitaxel Therapeutic Effects Towards PC-3 Prostate Cancer Through ER Stress Induction and ROS Production</p>

LncRNA MAFG‐AS1 facilitates the migration and invasion of NSCLC cell via sponging miR‐339‐5p from MMP15

RP11‐81H3.2 promotes gastric cancer progression through miR‐339‐HNRNPA1 interaction network

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