Foxo3a-Mediated DNMT3B Impedes Cervical Cancer Cell Proliferation and Migration Capacities through Suppressing PTEN Promoter Methylation

Li, Hongying; Yuan, Yuqin; Hong, Daojun; Wang, Tinghui; Zhang, Dunlan; Zhou, Limin; Chen, Lu; He, Xiufeng

doi:10.1080/08941939.2022.2162170

Cited by 5 publications

(2 citation statements)

References 31 publications

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“…This enzyme is responsible for the addition of methyl groups to DNA molecules, thereby influencing gene expression and cellular genomic stability. The abnormal activity of DNMT3B has been implicated in the occurrence and development of diverse cancers, specifically encompassing cervical cancer [12], breast cancer [13], endometrial cancer [14], and gastric cancer [15]. It induces abnormal DNA methylation, affecting the expression of tumor suppressor genes and oncogenes, consequently propelling tumor growth and advancement.…”

Section: Introductionmentioning

confidence: 99%

Methyltransferase DNMT3B promotes colorectal cancer cell proliferation by inhibiting PLCG2

Ji,

Wang,

Zou

et al. 2024

Preprint

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Background: Aberrant DNA methylation patterns in the promoter region of PLCG2 have been associated with dysregulated signaling pathways and cellular functions. Its role in colorectal cancer cells is still unknown. Methods: qRT-PCR was used to examine DNMT3B expression in colorectal cancer. Western blot and immunohistochemistry were used to analyze DNMT3B and PLCG2 protein levels in colorectal tissues and cell lines. The cell counting kit-8 and colony experiments were used to identify the proliferation of colorectal cancer cells. Methylation-specific PCR (MSP) and bisulfite-sequencing PCR (BSP) was used to measure DNA methylation levels. Results: DNMT3B is overexpressed in colorectal cell in TCGA datasets and Kaplan-Meier plots. DNMT3B is significantly overexpressed in tumor tissues compared to adjacent non-tumor tissues. Western blotting results demonstrated high expression of DNMT3B in tumor tissues. Compared to normal colonic epithelial cells, colorectal cancer cell lines exhibited elevated levels of PLCG2 methylation. oePLCG2 effectively prevented the in vivo xenograft tumor growth of colorectal cancer. Conclusions: PLCG2 is identified as a key downstream regulatory protein of DNMT3B in colorectal cancer. DNMT3B Inhibits PLCG2 transcription through methylation of the PLCG2 promoter region. DNMT3B controls colorectal cancer cell proliferation through the PLCG2, which is useful for creating therapeutic approaches that target PLCG2 expression for the treatment of colorectal cancer.

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Section: Introductionmentioning

confidence: 99%

Methyltransferase DNMT3B promotes colorectal cancer cell proliferation by inhibiting PLCG2

Ji,

Wang,

Zou

et al. 2024

Preprint

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“…These therapies are only effective in cases of early-stage cervical cancer. However, they have limited efficacy in the middle-advanced stage or metastatic cervical cancer because of their drug resistance, metastases, and so on [ 10 , 11 ]. Consequently, there is an urgent demand to seek novel biomarkers for better diagnosis and treatment of cervical cancer.…”

Section: Introductionmentioning

confidence: 99%

LncRNA ABHD11-AS1 activates EGFR signaling to promote cervical cancer progression by preventing FUS-mediated degradation of ABHD11 mRNA

Yang,

Tian,

Zhao

et al. 2023

Cell Cycle

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Cervical cancer is one of the most common gynecological cancers with high metastasis, poor prognosis and conventional chemotherapy. The long non-coding RNA (lncRNA) ABHD11 antisense RNA 1 (ABHD11-AS1) plays a vital role in tumorigenesis and is involved in cell proliferation, differentiation, and apoptosis. Especially for cervical cancer, the functions and mechanisms of ABHD11-AS1 are still undetermined. In this study, we explored the role and underlying mechanism of ABHD11-AS1 in cervical cancer. We found that ABHD11-AS1 is highly expressed in cervical cancer tissue. The roles of ABHD11-AS1 and EGFR have investigated the loss of function analysis and cell movability in SiHa and Hela cells. Knockdown of ABHD11-AS1 and EGFR significantly inhibited the proliferation, migration, and invasion and promoted apoptosis of SiHa and Hela cells by up-regulating p21 and Bax and down-regulating cyclin D1, Bcl2, MMP9, and Vimentin. ABHD11-AS1 knockdown could decrease the expression of EGFR. In addition, ABHD11-AS1 could regulate the EGFR signaling pathway, including p-EGFR, p-AKT, and p-ERK. Spearman’s correlation analysis and cell experiments demonstrated that ABHD11 was highly expressed in tumor tissue and partially offset the effect of shABHD11-AS1 on the proliferation, migration, and invasion of SiHa and Hela cells. Then, RNA pulldown was used to ascertain the mechanisms of ABHD11-AS1 and FUS. ABHD11-AS1 inhibited ABHD11 mRNA degradation by bounding to FUS. A subcutaneous xenograft of SiHa cells was established to investigate the effect of ABHD11-AS1 in tumor tissue. Knockdown of ABDH11-AS1 inhibited tumor growth and decreased the tumor volume. ABHD11-AS1 knockdown inhibited the expression of Ki67 and Vimentin and up-regulated the expression of Tunel. Our data indicated that ABHD11-AS1 promoted cervical cancer progression by activating EGFR signaling, preventing FUS-mediated degradation of ABHD11 mRNA. Our findings provide novel insights into the potential role of lncRNA in cervical cancer therapy.

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Virtual screening of FOXO3a activators from natural product-like compound library

et al. 2023

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Foxo3a-Mediated DNMT3B Impedes Cervical Cancer Cell Proliferation and Migration Capacities through Suppressing PTEN Promoter Methylation

Cited by 5 publications

References 31 publications

Methyltransferase DNMT3B promotes colorectal cancer cell proliferation by inhibiting PLCG2

Methyltransferase DNMT3B promotes colorectal cancer cell proliferation by inhibiting PLCG2

LncRNA ABHD11-AS1 activates EGFR signaling to promote cervical cancer progression by preventing FUS-mediated degradation of ABHD11 mRNA

Virtual screening of FOXO3a activators from natural product-like compound library

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