RETRACTED ARTICLE: Propofol inhibits migration and induces apoptosis of pancreatic cancer PANC-1 cells through miR-34a-mediated E-cadherin and LOC285194 signals

Wang, Hongwei; Jiao, Hongmei; Jiang, Ziru; Chen, Renyi

doi:10.1080/21655979.2020.1754038

Cited by 26 publications

(20 citation statements)

References 60 publications

(72 reference statements)

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“…Cyclin D1 is a nuclear factor of cell cycle, which can induce cell proliferation [ 29 ]; Bcl-2, as a member of the Bcl family, inhibited the cell apoptosis. While the trend of Bax is opposite to that of Bcl-2, which is a kind of a pro apoptotic factor [ 30 ]. In this study, we confirmed that knockdown of REV7 further down-regulated the expressions of Cyclin D1 and Bcl-2, and up-regulated the Bax expression.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of DNA polymerase ζ relieved the chemoresistance of glioma via inhibiting the PI3K/AKT signaling pathway

et al. 2021

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Previous reports suggest that DNA polymerase ζ is highly expressed in glioma tissues. The present study aimed to investigate the roles of the REV7 subunit of DNA polymerase ζ in glioma cell chemoresistance and its underlying mechanisms. The bioinformatics method was used to compare the expression of REV7 in glioma and normal tissues. The expression of REV7 in glioma tumor samples and the adjacent tissue was examined by reverse transcription polymerase chain reaction. Moreover, an in vitro analysis using glioma cells was used to test the effects of REV7 siRNA on the proliferation and apoptosis of glioma cell line U251 cells, and the effect of REV7 siRNA on the sensitivity of the U251 cells to cisplatin was also explored. The expression of REV7 in glioma tumors was significantly increased. Moreover, the knockdown of REV7 in glioma cells decreased the proliferation and increased the apoptosis of U251 cells; moreover, REV7 siRNA also increased the sensitivity of U251 cells to cisplatin. Finally, REV7 may regulate the proliferation, apoptosis, and chemosensitivity of U251 cells by affecting phosphoinositide 3-kinase signaling. Our data suggest that REV7 is involved in the chemosensitivity of glioma cells and provides a theoretical basis for targeting DNA polymerase ζ to improve the sensitivity of glioma cells to chemotherapy.

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Section: Discussionmentioning

confidence: 99%

Knockdown of DNA polymerase ζ relieved the chemoresistance of glioma via inhibiting the PI3K/AKT signaling pathway

et al. 2021

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“…With the advancement of anesthesia techniques, recent studies mainly focus on potential biological roles of anesthetics in tumor development. For instance, propofol showed its antitumor activity in pancreatic cancer cells by affecting miR-34a-mediated LOC285194 and E-cadherin signals [19]. Fentanyl is a commonly used as an anesthesia that exerts its antitumor effects in many human cancers.…”

Section: Discussionmentioning

confidence: 99%

Fentanyl Exerts an Antitumor Effect on Papillary Thyroid Cancer by Regulating the miR-204/KLF5 Axis

Jiang

Dai

et al. 2021

Journal of Nanomaterials

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Fentanyl is a strong anesthetic analgesic drug that plays important roles in many types of cancers. However, the role of fentanyl in papillary thyroid cancer (PTC) tumor development remains ambiguous. In this study, we aimed to investigate the potential antitumor effects of fentanyl on PTC cell viability and invasion. Results of cell counting kit-8 and Transwell assays demonstrated that fentanyl treatment (5 ng/ml) reduced the viability and invasion of two PTC cells, TCP-1 and BCPAP. Our data subsequently showed that fentanyl induced antitumor effects by increasing miR-204 expressions. Furthermore, the results of luciferase reporter assays identified that miR-204 directly targets Krüppel-like transcription factor 5 (KLF5), which serves as tumor-promoting genes in many cancers. Further mechanistic analyses revealed that fentanyl performs its tumor-suppressive functions by regulating the miR-204/KLF5 axis in PTC cells. These results contribute to understanding the important role of fentanyl in treating PTC.

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“…Identifying the mechanisms that regulate VSMC apoptosis potentially may lead to novel therapeutic approaches that are more efficacious for these patients. Previous works showed that LOC285194 overexpression induced cell apoptosis in gastric carcinoma [ 28 ], pancreatic cancer [ 29 ] and colon cancer [ 10 ]. In the present study, we demonstrated that LOC285194 overexpression significantly induced A7r5 cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA LOC285194 inhibits proliferation and migration but promoted apoptosis in vascular smooth muscle cells via targeting miR-211/PUMA and TGF-β1/S100A4 signal

Wang

et al. 2020

Bioengineered

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Long non-coding RNA LOC285194 (LOC285194) has reported to regulate vascular smooth muscle cells (VSMCs) proliferation and apoptosis in vitro and in vivo . Here we aimed to determine the role of LOC285194 in the proliferation, migration and apoptosis of VSMCs and its underlying mechanisms. A7r5 cells were transfected with Lv-LOC285194 or control Lv-NC for 24–72 h, or small interfering RNA targeting S100A4 (S100A4 siRNA) for 24–48 h, or co-transfected with Lv-LOC285194 and PUMA siRNA for 72 h, or treated with miR-211 inhibitor or co-transfected with Lv-LOC285194 and miR-211 mimics for 72 h. A7r5 cells were also treated with transforming growth factor – β(TGF-β) (5 ng/ml) after Lv-LOC285194 transfection for 24 h. The relationship between LOC285194 and TGF-β was confirmed using luciferase reporter assay. Cell proliferation and cell apoptosis were analyzed by Cell Counting Kit-8 (CCK-8) assay, ELISA and TUNEL staining. LOC285194 and miR-211 expression were detected by qPCR assay. S100A4, pro-apoptotic and anti-apoptotic protein were detected by Western blot assay. LOC285194 inhibited cell proliferation, invasion and migration and promoted cell apoptosis accompanied by upregulation of PUMA and downregulation of miR-211 and S100A4. Targeting PUMA reversed the effect of LOC285194 on cell apoptosis and proliferation. miR-211 mimic inhibited LOC285194-induced PUMA upregulation and decreased LOC285194-induced cell apoptosis. TGF-β (5 ng/ml) treatment reversed S100A4 siRNA or LOC285194-induced S100A4 expression. Luciferase reporter assay showed that TGF-β was the target of LOC285194. LOC285194 inhibits proliferation and promoted apoptosis in vascular smooth muscle cells via targeting miR-211/PUMA signal; In addition, LOC285194 decreased cell invasion and migration by targeting TGF-β1/S100A4 signal.

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RETRACTED ARTICLE: Propofol inhibits migration and induces apoptosis of pancreatic cancer PANC-1 cells through miR-34a-mediated E-cadherin and LOC285194 signals

Cited by 26 publications

References 60 publications

Knockdown of DNA polymerase ζ relieved the chemoresistance of glioma via inhibiting the PI3K/AKT signaling pathway

Knockdown of DNA polymerase ζ relieved the chemoresistance of glioma via inhibiting the PI3K/AKT signaling pathway

Fentanyl Exerts an Antitumor Effect on Papillary Thyroid Cancer by Regulating the miR-204/KLF5 Axis

Long non-coding RNA LOC285194 inhibits proliferation and migration but promoted apoptosis in vascular smooth muscle cells via targeting miR-211/PUMA and TGF-β1/S100A4 signal

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