Overexpressing miR‑335 inhibits DU145 cell proliferation by targeting early growth response 3 in prostate cancer

Zhang, Peng; Yang, Xiaojie; Wang, Li; Zhang, Dong; Luo, Qidong; Wang, Binxian

doi:10.3892/ijo.2019.4778

Cited by 16 publications

(16 citation statements)

References 65 publications

(66 reference statements)

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“…miR-335-5p has been related to certain types of cancer. [24][25][26] miR-335-5p inhibits cell proliferation, migration and invasion in colorectal cancer through downregulating LDHB. 27 miR-335-5p targeting ICAM-1 inhibits invasion and metastasis of thyroid cancer cells.…”

Section: Discussionmentioning

confidence: 99%

<p>miR-335-5p Regulates Cell Cycle and Metastasis in Lung Adenocarcinoma by Targeting CCNB2</p>

Wang¹,

Xiao²,

Wu³

et al. 2020

OTT

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Background: Lots of studies have shown that cyclin disorders can promote tumor development. This study aims to investigate the biological function and molecular mechanism of CCNB2 in lung adenocarcinoma (LUAD). Methods: LUAD data were downloaded from GEO database and TCGA-LUAD database. Differential analysis was conducted to find the differentially expressed miRNAs and mRNAs, while targeted prediction was done for the access of potential target mRNAs. Gene expression level was detected by qRT-PCR and Western blot in human LUAD cell lines A-427, A549, Calu-3, PC-9 and human bronchial epithelial cell line BEAS-2B. MTT, colony formation, Transwell and flow cytometry assays were used to detect cell proliferation, metastasis, and cell cycle changes of PC-9 cell line. The dual-luciferase reporter gene was used to detect the targeted binding relationship of the target miRNA and mRNA. Results: CCNB2 was highly expressed and served as a biomarker indicating poor prognosis in LUAD patients. Cell function experiments confirmed the inhibitory effects of silencing CCNB2 on the proliferation, migration and invasion of LUAD cells and cell cycle was blocked in the G0/G1 phase. In addition, with regard to the regulatory mechanism, we demonstrated that miR-335-5p had binding sites with 3ʹ-UTR of CCNB2, indicating that miR-335-5p could target the regulation expression of CCNB2. In subsequent cell function tests, overexpression of miR-335-5p inhibited the proliferation and metastasis of cancer cells, and the rescue experiments also verified that miR-335-5p could reverse the promotion of CCNB2 overexpression on the progress of cancer cells. Conclusion: In summary, our results revealed that miR-335-5p could target the downregulation of CCNB2 to inhibit the occurrence and development of LUAD.

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Section: Discussionmentioning

confidence: 99%

<p>miR-335-5p Regulates Cell Cycle and Metastasis in Lung Adenocarcinoma by Targeting CCNB2</p>

Wang¹,

Xiao²,

Wu³

et al. 2020

OTT

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“…Previous studies reported that EGR3 was ubiquitously expressed in the cerebral cortex, substrate ganglion and neuromuscular spindle (13). Increased EGR3 expression induced expression of IL-6 and IL-8 has been previously demonstrated in prostate cancer (29), suggesting that EGR3 also serves an important role in tumorigenesis. Of note, EGR3 were also shown to be downregulated in glioma tissues in comparison with adjacent normal tissues, and EGR3 knockdown in vitro promoted glioma cell proliferation.…”

Section: Discussionmentioning

confidence: 71%

miR‑454‑3p promotes of human glioma cell growth by targeting EGR3

Shen

Mou

et al. 2019

Exp Ther Med

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Gliomas are the most common primary brain tumors in adults and are associated with high mortality rates. In the present study, the aim was to evaluate the role of miR-454-3p in the pathogenesis of human glioma and to explore the underlying mechanism. Reverse transcription-quantitative PCR was performed to compare the expression levels of miR-454-3p in glioma and adjacent normal tissue. The effects of miR-454-3p on cell proliferation was tested by combining MTT and colony formation assays. Dual-luciferase assay was used to identify the target gene of miR-454-3p. The results showed that miR-454-3p was upregulated in glioma tissues where it exerts a positively regulatory role on cell growth. Dual-luciferase assay confirmed Early Growth Response 3 (EGR3) to be a target for miR-454-3p. Overexpression of EGR3 in glioma cells was found to impair miR-454-3p mimic-induced cell proliferation. These results suggested that upregulated miR-454-3p served an important role in glioma tumorigenesis by targeting EGR3, which provided valuable insights into the underlying mechanism of the disease that may lead to possible novel therapeutic strategies.

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“…Previous reports have shown that PE exhibits broad spectrum significant inhibition activity against some tumor cell lines in vitro, such as PC-3, A549, LoVo, MCF-7, HL-60, VA-13, HepG2, HONE-1, NUGC-3, SGC-7901, BGC-823, and MKN-45 [5,[8][9][10][11][12]17]. In addition, the efficacy of PE was also examined using SGC-7901 and A549 xenograft mice in vivo [17,18].…”

Section: Discussionmentioning

confidence: 99%

“…Thus, investigating the effect of PE on the apoptosis and autophagy of PCa cells can aid in elucidating the anti-PCa effect of PE. The DU145 cell line is not measurably hormone-sensitive and is typically used as the standard PCa cell line in research [12]. To date, there is no report on whether PE has an effect on human PCa DU145 cells in vitro and in vivo.…”

Section: Introductionmentioning

confidence: 99%

Peperomin E Induces Apoptosis and Cytoprotective Autophagy in Human Prostate Cancer DU145 Cells In Vitro and In Vivo

Lin

Zhu

et al. 2021

Planta Med

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Peperomin E was first isolated from Peperomia dindygulensis, an anticarcinogenic herb, and exhibited anticancer activity in many cancer cell lines. To date, it is unknown whether peperomin E has an effect on human prostate cancer DU145 cells in vitro and in vivo. In this study, we used MTT to assess the proliferation inhibition activity of peperomin E in DU145 cells in vitro and observed the cell morphological changes by a phase contrast microscope. A DU145 cell xenograft tumor mouse model was used to evaluate the efficacy of peperomin E in vivo. Apoptosis rates were measured by flow cytometry, and protein expression levels were analyzed by western blot. The results showed that peperomin E significantly inhibited the proliferation of DU145 cells in vitro and reduced the weight and volume of tumors in vivo. Peperomin E also significantly induced the apoptosis and autophagic response of DU145 cells. The autophagic inhibitors LY294002 and chloroquine enhanced peperomin E-mediated inhibition of DU145 cell proliferation and induction of DU145 cell apoptosis. The results also showed that the Akt/mTOR pathway participated in peperomin E-induced autophagy in DU145 cells. In summary, our finding showed that peperomin E had an effect on DU145 cells in vitro and in a nude mouse DU145 cell xenograft model in vivo, demonstrated that peperomin E could significantly induce apoptosis and the autophagic response in DU145 cells and that autophagy played a cytoprotective role in peperomin E-treated DU145 cells. These results suggest that the combination of peperomin E treatment and autophagic inhibition has potential for the treatment of prostate cancer.

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Overexpressing miR‑335 inhibits DU145 cell proliferation by targeting early growth response 3 in prostate cancer

Cited by 16 publications

References 65 publications

<p>miR-335-5p Regulates Cell Cycle and Metastasis in Lung Adenocarcinoma by Targeting CCNB2</p>

<p>miR-335-5p Regulates Cell Cycle and Metastasis in Lung Adenocarcinoma by Targeting CCNB2</p>

miR‑454‑3p promotes of human glioma cell growth by targeting EGR3

Peperomin E Induces Apoptosis and Cytoprotective Autophagy in Human Prostate Cancer DU145 Cells In Vitro and In Vivo

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