GRSF1-mediatedMIR-G-1promotes malignant behavior and nuclear autophagy by directly upregulatingTMED5andLMNB1in cervical cancer cells

Yang, Zhen; Sun, Qi; Guo, Junfei; Wang, Shixing; Song, Ge; Liu, Weiying; Liu, Min; Tang, Hua

doi:10.1080/15548627.2018.1539590

Cited by 86 publications

(69 citation statements)

References 67 publications

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“…However, research has con rmed that NST could not cure cancer. On the contrary, starvation makes cancer cells adapt to adverse conditions, and the surviving cells become more aggressive via EMT [5,26]. Our study con rmed that NST and silencing Akt1 promoted the EMT process of PCa cells.…”

Section: Discussionsupporting

confidence: 58%

Silencing Akt1 Inhibits Starvation Induced Lung Metastasis Through Epithelial Mesenchymal Transition Independent of E-cadherin in Prostate Cancer

Yang¹,

Liu²,

Qiu³

et al. 2020

Preprint

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BackgroundEpithelial to mesenchymal transition (EMT) of prostate cancer (PCa) cells facilitates their progress to metastasis. We have recently reported Akt1 is an important EMT regulator, and silencing Akt1 induced EMT and inhibited the growth of PCa cells. These results imply Akt1 silencing may increase starvation resistance of PCa cells. However, little is known about the role of Akt1 of PCa cells in starvation.MethodsApoptosis was detected by TUNEL and flow cytometry, cell invasion was detected by transwells and ECIS, lung metastasis was evaluated by tail vein injection animal model, variation of EMT markers was detected by Western-blot.ResultsWe found starvation slowed down the growth and proliferation, and increased apoptosis of PCa cells; Silencing Akt1 gene inhibited these effects of starvation and decreased E-cadherin. Akt1 silencing enhanced invasion induced by starvation of PCa cells in vitro ; however, it inhibited lung metastasis induced by starvation of PCa cells in vivo unexpectedly.ConclusionStarvation or silencing Akt1 alone can promote lung metastasis of PCa cells, however, silencing Akt1 while starving PCa cells can significantly inhibit this function via EMT independent of E-cadherin.

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Section: Discussionsupporting

confidence: 58%

Silencing Akt1 Inhibits Starvation Induced Lung Metastasis Through Epithelial Mesenchymal Transition Independent of E-cadherin in Prostate Cancer

Yang¹,

Liu²,

Qiu³

et al. 2020

Preprint

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“…5 Lamins, which are divided into A and B types, are located in the nuclear membrane and their main function is to stabilize the binding of protein and chromatin. 6 Recently, more and more studies have indicated that Lamin B1 are abnormally expressed in multiple types of tumors such as hepatocellular carcinoma, 7 colon cancer, 8 cervical cancer 9 and breast cancer. 10 These studies indicate that Lamin B1 can be used clinically as a novel tumor biomarker to guide physicians in developing treatment strategies and accurately predicting patient outcomes.…”

Section: Introductionmentioning

confidence: 99%

“…It indicated that overexpression of Lamin B1 might play an of vital role in malignant behavior of cervical cancer cells. 9 Except that, the AKT pathway plays a key role in the regulation of multiple cellular life activities such as proliferation survival, invasion and differentiation. 11 Many tumors including lung cancer promotes tumorigenesis and inhibits apoptotic signals by activating AKT pathway.…”

Section: Introductionmentioning

confidence: 99%

Lamin B1 Overexpresses in Lung Adenocarcinoma and Promotes Proliferation in Lung Cancer Cells via AKT Pathway

Li¹,

Li²,

Li³

et al. 2020

OTT

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These authors contributed equally to this workPurpose: This study aims to investigate the biological effect and molecular mechanism of Lamin B1(LMNB1) in lung cancer cells and its significance for the prognosis of lung adenocarcinoma(LUAD) patients. Methods: In this study, Bioinformatics was performed to analyze the expression at mRNA level and prognosis effect of LMNB1 in LUAD from TCGA dataset. The immunohistochemistry(IHC) assay was conducted to analyzed the expression of LMNB1 at the protein level in LUAD tissues. The correlation between the expression of LMNB1 and the clinical factors in patients with LUAD was analyzed. Next, LMNB1 transfected into LUAD cell lines (A549 and PC-9) which was proved by Western blot. CCK8 assay, cloning formation assay, and xenograft assay were conducted to explore the effect and mechanism of LMNB1 on the proliferation of LUAD cell lines in vitro and in vivo. Results:The results of the present study demonstrated that LMNB1 was highly expressed in LUAD tissues and related to tumor stage. High LMNB1 expression was related with more advanced clinicopathological factors such as low degree of differentiation (P=0.02), large tumor size (P<0.01), lymph node metastasis (P<0.01) and higher tumor stage (P<0.01). After knocking down LMNB1, the cell growth rate (P<0.01) and the number of colonies (P<0.01) were significantly reduced, and the level of the proliferating marker Ki67 (P<0.01) was significantly decreased. At the same time, in vivo experiments showed that the tumor volume and tumor of the mice were significantly reduced (P<0.01). Moreover, we found that knockdown LMNB1 can inhibit the proliferation of lung cancer cells by inhibiting AKT phosphorylation by Western blot. Conclusion: In summary, LMNB1 play an of vital roles in the growth of LUAD cells, highlighting its potential as a therapeutic target for the treatment of LUAD patients.

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“…circRNA hsa_circ_0023404 was significantly upregulated in CC tissues compared to adjacent normal tissues. And, it enhances cervical cancer metastasis and chemoresistance through vascular endothelial growth factor A (VEGFA) and autophagy signaling by sponging miR‐5047 . GRSF1 (G‐rich RNA sequence binding factor 1) was originally identified as an RNA‐binding protein with high affinity for G‐rich sequences.…”

Section: Introductionmentioning

confidence: 99%

“…And, it enhances cervical cancer metastasis and chemoresistance through vascular endothelial growth factor A (VEGFA) and autophagy signaling by sponging miR-5047. 93 GRSF1 (G-rich RNA sequence binding factor 1) was originally identified as an RNA-binding protein with high affinity for Grich sequences. MIR-G-1 upregulates TMED5 and lamin B1 (LMNB1) in a GRSF1-dependent manner and promotes malignant behavior and nuclear autophagy in the cervical cancer cells.…”

mentioning

confidence: 99%

MicroRNAs play an essential role in autophagy regulation in various disease phenotypes

et al. 2019

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Autophagy is a highly conserved catabolic process and fundamental biological process in eukaryotic cells. It recycles intracellular components to provide nutrients during starvation and maintains quality control of organelles and proteins. In addition, autophagy is a well‐organized homeostatic cellular process that is responsible for the removal of damaged organelles and intracellular pathogens. Moreover, it also modulates the innate and adaptive immune systems. Micro ribonucleic acids (microRNAs) are a mature class of post‐transcriptional modulators that are widely expressed in tissues and organs. And, it can suppress gene expression by targeting messenger RNAs for translational repression or, at a lesser extent, degradation. Research indicates that microRNAs regulate autophagy through different pathways, playing an essential role in the treatment of various diseases. It is an important regulator of fundamental cellular processes such as proliferation, autophagy, and cell apoptosis. In this review article, we first review the current knowledge of autophagy and the function of microRNAs. Then, we summarize the mechanism of autophagy and the signaling pathways related to autophagy by citing at least the main proteins involved in the different phases of the process. Second, we introduce other members of RNA and report some examples in various pathologies. Finally, we review the current literature regarding microRNA‐based therapies for cancer, atherosclerosis, cardiac disease, tuberculosis, and viral diseases. MicroRNAs can cause autophagy upregulation or downregulation by targeting genes or affecting autophagy‐related signaling pathways. Therefore, the microRNAs have a huge potential in autophagy regulation, and it is the function as diagnostic and prognostic markers.

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GRSF1-mediatedMIR-G-1promotes malignant behavior and nuclear autophagy by directly upregulatingTMED5andLMNB1in cervical cancer cells

Cited by 86 publications

References 67 publications

Silencing Akt1 Inhibits Starvation Induced Lung Metastasis Through Epithelial Mesenchymal Transition Independent of E-cadherin in Prostate Cancer

Silencing Akt1 Inhibits Starvation Induced Lung Metastasis Through Epithelial Mesenchymal Transition Independent of E-cadherin in Prostate Cancer

<p>Lamin B1 Overexpresses in Lung Adenocarcinoma and Promotes Proliferation in Lung Cancer Cells via AKT Pathway</p>

MicroRNAs play an essential role in autophagy regulation in various disease phenotypes

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