自引率: 1%
被引量: 2775
通过率: 暂无数据
审稿周期: 1.07
版面费用: 暂无数据
国人发稿量: 37
期刊描述简介:
Oncogenesis is a peer-reviewed open access online journal that publishes full-length papers, reviews, and short communications exploring the molecular basis of cancer and related phenomena. It seeks to promote diverse and integrated areas of molecular biology, cell biology, oncology, and genetics. Oncogenesis seeks to encompass the breadth of the molecular biology of malignant change, and topics of particular interest include: Apoptosis Cancer metabolism Cell cycle and growth regulation Cellular oncogenes Cellular transformation and immortalization DNA damage and repair Mode of action of cancer therapeutics Molecular oncology Novel targeted therapies Senescence Tumour suppression Virus-induced oncogenesis
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Tumor suppressor BAP1 suppresses disulfidptosis through the regulation of SLC7A11 and NADPH levels.
被引量：- 发表：1970
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Correction: Dihydroartemisinin inhibits prostate cancer via JARID2/miR-7/miR-34a-dependent downregulation of Axl.
被引量：- 发表：1970
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TFCP2L1 drives stemness and enhances their resistance to Sorafenib treatment by modulating the NANOG/STAT3 pathway in hepatocellular carcinoma.
被引量：- 发表：1970
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Peptidylarginine deiminase 3 modulates response to neratinib in HER2 positive breast cancer.
被引量：- 发表：1970
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Combined Inhibition of PI3K and STAT3 signaling effectively inhibits bladder cancer growth.
Bladder cancer is characterized by aberrant activation of the phosphatidylinositol-3-OH kinase (PI3K) signaling, underscoring the significance of directing therapeutic efforts toward the PI3K pathway as a promising strategy. In this study, we discovered that PI3K serves as a potent therapeutic target for bladder cancer through a high-throughput screening of inhibitory molecules. The PI3K inhibitor demonstrated a robust anti-tumor efficacy, validated both in vitro and in vivo settings. Nevertheless, the feedback activation of JAK1-STAT3 signaling reinstated cell and organoid survival, leading to resistance against the PI3K inhibitor. Mechanistically, the PI3K inhibitor suppresses PTPN11 expression, a negative regulator of the JAK-STAT pathway, thereby activating STAT3. Conversely, restoration of PTPN11 enhances the sensitivity of cancer cells to the PI3K inhibitor. Simultaneous inhibition of both PI3K and STAT3 with small-molecule inhibitors resulted in sustained tumor regression in patient-derived bladder cancer xenografts. These findings advocate for a combinational therapeutic approach targeting both PI3K and STAT3 pathways to achieve enduring cancer eradication in vitro and in vivo, underscoring their promising therapeutic efficacy for treating bladder cancer.
被引量：- 发表：1970
