Upregulation of miR‐874‐3p and miR‐874‐5p inhibits epithelial ovarian cancer malignancy via SIK2

Xia, Bairong; Mei, Lin; Dong, Wei; Chen, Hong; Li, Bing; Zhang, Xiaye; Hou, Yan; Lou, Ge

doi:10.1002/jbt.22168

Cited by 46 publications

(37 citation statements)

References 36 publications

(42 reference statements)

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“…Our research found that when the SIK2 expression in BC cells was silenced, their proliferation, invasion and aerobic glycolysis ability enhanced significantly, while the opposite phenomenon was observed after the SIK2 expression increased further. Previous studies [21] have found that inhibiting the expression of SIK2 can inhibit the growth of ovarian cancer cells, suggesting that SIK2 was effective as a oncogene, which is similar to our conclusion. Subsequently, to investigate the effect of SIK2 on DDP resistance of BC cells, we established a cisplatin-resistant cell line and analyzed the sensitivity of SIK2 to DDP in cells after intervention.…”

Section: Discussionsupporting

confidence: 92%

SIK2 Promotes Cisplatin Resistance Induced by Aerobic Glycolysis in Breast Cancer Cells through PI3K/AKT/mTOR Signaling Pathway

Zong

Dai

Fang

et al. 2020

Preprint

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Objective This study aimed to investigate the effect of SIK2 on cisplatin resistance induced by aerobic glycolysis in breast cancer cells and its potential mechanism. Methods qRT-PCR and Western blot were used to detect SIK2 mRNA and protein levels. Cisplatin (DDP) resistant cell lines of breast cancer cells were established, CCK-8 was used to measure and evaluate the viability, and Transwell was used to evaluate the cell invasion capability. Flow cytometry was adopted to evaluate the apoptosis rate. The glycolysis level was evaluated by measuring glucose consumption and lactic acid production. The protein levels of p-PI3K, p- protein kinase B (Akt) and p-mTOR were determined by western blot. Results SIK2 is highly expressed in breast cancer tissues and cells compared with adjacent tissues and normal human breast epithelial cells, and has higher diagnostic value for breast cancer. Silencing SIK2 expression can inhibit proliferation and invasion of breast cancer cells and induce their apoptosis. In addition, SIK2 knockdown inhibits glycolysis, reverses the resistance of drug-resistant cells to cisplatin, and inhibits PI3K/AKT/mTOR signaling pathway. When LY294002 is used to inhibit PI3K/AKT/mTOR signaling pathway, the effect of Sh-SIK2 on aerobic glycolysis of breast cancer cells can be reversed. Conclusion SIK2 can promote cisplatin resistance caused by aerobic glycolysis of breast cancer cells through PI3K/AKT/mTOR signaling pathway, which may be a new target to improve cisplatin resistance of breast cancer cells.

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Section: Discussionsupporting

confidence: 92%

SIK2 Promotes Cisplatin Resistance Induced by Aerobic Glycolysis in Breast Cancer Cells through PI3K/AKT/mTOR Signaling Pathway

Zong

Dai

Fang

et al. 2020

Preprint

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“…Identification of ERN1 is noteworthy given that during the ER stress response, this gene encodes the ER stress sensor inositol-requiring enzyme 1 (IRE1a), responsible for the unconventional cleavage of a 26 nucleotide fragment from Xbp1 mRNA, resulting in the generation of the active spliced variant of XBP1 (XBP1s) and enabling it to function as a potent transcription factor (17). Additional candidate drivers in fetal bone marrow following maternal OM-85 treatment included CD38, IL5 and an array of microRNAs (miR) ( Figure 3A right panel; Supplemental Table 5) recognised principally in the context of cancer-associated functions (18)(19)(20). It is important to note however, that miR-149-3p has been shown to negatively regulate Toll-like receptor (TLR) 4 expression in murine monocytic cells in vitro (21) and it is possible that other miRs may have similar (but as yet undefined) innate immune regulatory functions (22).…”

Section: Resultsmentioning

confidence: 99%

Transplacental innate immune training via maternal microbial exposure: the XBP1-ERN1 axis in programming dendritic cell precursors

Mincham

Jones

Bodinier

et al. 2019

Preprint

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Non-pathogenic environmental microbial exposures during pregnancy can be transplacentally transcribed into beneficial immune training signals for the developing fetus.These signals equip offspring for more rapid adaptation to the microbe-rich postnatal environment by optimising immunoregulatory innate cell function. We have previously identified that maternal treatment with a microbial-derived therapeutic (OM-85) can protect offspring against allergic airways inflammation. Here, we show that oral treatment of pregnant mice with OM-85 induces transplacental signals that manifest in fetal bone marrow as an enriched population of conventional dendric cells (cDC) displaying enhanced functional maturation. Moreover, the myeloid progenitor populations directly upstream of this cDC pool were significantly boosted in response to maternal treatment. Transcriptomic analysis of fetal bone marrow identified maternal OM-85-induced activation of X-box binding protein 1 (XBP1), with upregulation of active XBP1 restricted to cDC precursors. These data provide direct evidence that transplacental immune training with a microbial-derived therapeutic can accelerate functional immune competence of the fetal bone marrow myeloid compartment. KTM, PGH and DHS designed the study. KTM, MB , NMS and JFLJ performed the experiments. KTM, ACJ, MB and DHS analysed the data. PAS and AB contributed to the project design and discussions on data interpretation. KTM, PAS, PGH and DHS wrote the manuscript. All authors reviewed the final version of the manuscript.

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“…An increasing number of studies confirm that miRNAs participate in various tumors, such as with respect to tumor migration and proliferation. miR‐874‐3p expression is abnormally decreased in various cancers, including ovarian cancer, 19 colorectal cancer 20 and hepatocellular carcinoma 21 . Zhu et al 12 .…”

Section: Discussionmentioning

confidence: 99%

miR‐874‐3p inhibits cell migration through targeting RGS4 in osteosarcoma

Liu

Zhuo

Lü

et al. 2020

The Journal of Gene Medicine

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Background The present study explored the role and mechanism of microRNA‐874‐3p (miR‐874‐3p) in the migration of the osteosarcoma cell line, U‐2 OS. Methods The expression profile of osteosarcoma (OS) microRNA (GSE65071) datasets was downloaded from the Gene Expression Omnibus (GEO) database (https://www.ncbi.nlm.nih.gov/geo) to identify differentially expressed miRNAs in OS and its biological functions. A quantitative reverse transcription‐polymerase chain reaction was performed to detect the expression of miR‐874‐3p and its target gene regulator of G protein 4 (RGS4) in human osteosarcoma cells U‐2 OS and normal osteoblast hFOB1.19. Plasmid overexpression miR‐874‐3p and pcDNA‐RGS4 were transfected into U‐2 OS using Lipofectamine 2000 (Thermo Fisher, Waltham, MA, USA). Cell migration was measured using Transwell migration assays. Bioinformatic analysis and luciferase reporter assay were conducted to search for the target gene of miR‐874‐3p. Results In total, 167 differentially expressed miRNAs were detected after the analysis of GSE65071; of which 78 were up‐regulated genes and 89 were down‐regulated. miR‐874‐3p was down‐regulated and selected for further analysis. The expression level of miR‐874‐3p in U‐2 OS cells was significantly decreased compared to the hFOB1.19 cell line (p < 0.05). Overexpression of miR‐874‐3p significantly inhibited the proliferation and migration of U‐2 OS cells and overexpression of RGS4 reversed the inhibitory effect of miR‐874‐3p on U‐2 OS cells. Through luciferase report analyses and bioinformatic analysis, RGS4 may be the candidate target gene of miR‐874‐3p. Conclusions In conclusion, overexpression of miR‐874‐3p suppressed OS cell proliferation and migration. Thus, miR‐874‐3p might present a therapeutic agent for the treatment of OS.

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Upregulation of miR‐874‐3p and miR‐874‐5p inhibits epithelial ovarian cancer malignancy via SIK2

Cited by 46 publications

References 36 publications

SIK2 Promotes Cisplatin Resistance Induced by Aerobic Glycolysis in Breast Cancer Cells through PI3K/AKT/mTOR Signaling Pathway

SIK2 Promotes Cisplatin Resistance Induced by Aerobic Glycolysis in Breast Cancer Cells through PI3K/AKT/mTOR Signaling Pathway

Transplacental innate immune training via maternal microbial exposure: the XBP1-ERN1 axis in programming dendritic cell precursors

miR‐874‐3p inhibits cell migration through targeting RGS4 in osteosarcoma

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