Last update 01 Nov 2024

PRC1 x Cytokines

Last update 01 Nov 2024

Basic Info

Related Targets

PRC1Cytokines

Drugs associated with PRC1 x Cytokines

BKT-300

Target

Cytokines x PRC1

Mechanism

Cytokines modulators [+1]

Active Org.

Hadassah-Hebrew University Hospital [+1]

Originator Org.

Biokine Therapeutics Ltd.

Active Indication

Neoplasms

Inactive Indication

Solid tumor

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with PRC1 x Cytokines

100 Translational Medicine associated with PRC1 x Cytokines

0 Patents (Medical) associated with PRC1 x Cytokines

Literatures (Medical) associated with PRC1 x Cytokines

01 Aug 2023·Immunity, Inflammation and Disease

E2F3 renders an immunosuppressive tumor microenvironment in nasopharyngeal carcinoma: Involvements of the transcription activation of PRC1 and BIRC5

Article

Author: Wang, Qiang ; Yu, Qi ; Liu, Yueyang

AbstractBackgroundE2F transcription factors are well‐recognized oncogenic molecules, and their correlation with immune cell infiltration has recently been reported. This work studies the impacts and mechanism of E2F transcription factor 3 (E2F3) in the growth and tumor microenvironment (TME) of nasopharyngeal carcinoma (NPC).MethodsAberrantly expressed transcription factors in NPC were screened by abundant bioinformatics analyses. Gene expression in NPC cells was analyzed by reverse transcription‐quantitative polymerase chain reaction and Western blot analyses. Malignant behaviors of NPC cells were analyzed by cell counting kit‐8, 5‐ethynyl‐2′‐deoxyuridine labeling, Transwell assays, and xenograft tumor models. TPA‐induced THP‐1 cells (macrophages) were cultured in the conditioned medium of NPC cells to mimic tumor‐associated macrophages (TAMs) in vivo, and these TAMs were cocultured with CD8+ T cells. Regulation of E2F3 on protein regulator of cytokinesis 1 (PRC1) and baculoviral IAP repeat containing 5 (BIRC5) was validated by chromatin immunoprecipitation and luciferase reporter assays.ResultsE2F3 was highly expressed in NPC cells, and its knockdown suppressed malignant behavior and tumorigenic ability of the cells. The E2F3 knockdown condition downregulated M2 cytokines CD163 and interleukin‐10 in TAMs, which further enhanced proliferation and activation of the cocultured CD8+ T cells. E2F3 promoted transcription of PRC1 and BRIC5. Furthermore, PRC1 or BRIC5 upregulation in NPC cells restored the malignant properties of NPC cells, reprogrammed the TAMs to M2 phenotype, and suppressed the CD8+ T cell proliferation and activation.ConclusionThis work suggests that E2F3 renders an immunosuppressive TME in NPC by activating PRC1 and BIRC5. Suppression of any member involved might favor tumor elimination.

01 Aug 2019·Cancer CellQ1 · MEDICINE

The Polycomb Repressor Complex 1 Drives Double-Negative Prostate Cancer Metastasis by Coordinating Stemness and Immune Suppression

Q1 · MEDICINE

Article

Author: Han, Hyun Ho ; Liang, Xin ; Su, Jie ; Cheng, Yuanming ; Rumandla, Alekya ; Yang, Guangli ; Chakraborty, Goutam ; Ouerfelli, Ouathek ; Wang, Guocan ; Scher, Howard I ; Zhou, Bing ; Giancotti, Filippo G ; Rosen, Neal ; Su, Wenjing ; Zhang, Boyu ; Wang, Yan ; Gurrapu, Sreeharsha

The mechanisms that enable immune evasion at metastatic sites are poorly understood. We show that the Polycomb Repressor Complex 1 (PRC1) drives colonization of the bones and visceral organs in double-negative prostate cancer (DNPC). In vivo genetic screening identifies CCL2 as the top prometastatic gene induced by PRC1. CCL2 governs self-renewal and induces the recruitment of M2-like tumor-associated macrophages and regulatory T cells, thus coordinating metastasis initiation with immune suppression and neoangiogenesis. A catalytic inhibitor of PRC1 cooperates with immune checkpoint therapy to reverse these processes and suppress metastasis in genetically engineered mouse transplantation models of DNPC. These results reveal that PRC1 coordinates stemness with immune evasion and neoangiogenesis and point to the potential clinical utility of targeting PRC1 in DNPC.

01 Mar 2019·Journal of Cancer Research and Clinical OncologyQ3 · MEDICINE

ZWINT is the next potential target for lung cancer therapy

Q3 · MEDICINE

Article

Author: Li, Qiang ; Bao, Yong ; Shen, Guo-Ping ; Peng, Fang ; Luo, Ying ; Niu, Shao-Qing ; Chen, Ming

PURPOSEWe aimed to analyze the expression of ZWINT, NUSAP1, DLGAP5, and PRC1 in tumor tissues and adjacent tissues with public data.METHODSThe expression patterns of four genes were detected in cancer tissues and adjacent tissues by qRT-PCR. The overall survival analysis was used to explore these genes in lung adenocarcinoma and squamous cell carcinoma patients. Knockdown assays were used to select the most suitable gene among these four genes. Cell function assays with the knockdown gene were conducted in A549 and NCL H226 cells. The role of the knockdown gene in lung cancer was dissected in a mice tumor model. Transcriptome sequencing analyses with the knockdown gene were analyzed.RESULTSOverexpression of these genes was significantly detected in cancer tissues (P < 0.01). Overall survival revealed that high expression of these genes is closely related with poor prognosis of lung adenocarcinoma patients (P < 0.05). Knockdown of ZWINT reduced proliferation in NCI H226 and A549 cells (P < 0.05). Knockdown also inhibited cell migration, invasion, apoptosis, and colony formation (P < 0.05). ZWINT knockdown reduced tumor volume (P < 0.05). Transcriptome sequencing of ZWINT knockdown-treated A549 and NCI H226 cells indicated that 100 and 426 differentially expressed genes were obtained, respectively. Gene ontology analysis suggested that binding, biological regulation, and multicellular organismal processes were the most enriched. KEGG analysis revealed that TNF, P53, and PI3K signal networks would be the most potential ZWINT-related pathways and were identified by Western blot analysis.CONCLUSIONSZWINT may be a novel target for lung cancer therapy.

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