2021
DOI: 10.3390/cancers13092168
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Abstract: Background: Despite recent advances in therapies, resistance to chemotherapy remains a critical problem in the clinical management of colorectal cancer (CRC). Cancer stem cells (CSCs) play a central role in therapy resistance. Thus, elimination of CSCs is crucial for effective CRC therapy; however, such strategies are limited. Autophagy promotes resistance to cancer therapy; however, whether autophagy protects CSCs to promote resistance to CRC-therapy is not well understood. Moreover, specific and potent autop… Show more

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Cited by 28 publications
(21 citation statements)
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“…The landscape of copy number aberrations and structural variations revealed potentially clinically exploitable deletion of TOX as a predictor for anti-PD1 response 107 , amplification of MALT1, whose inhibition has been shown to be selectively toxic for ABC-DLBCL 152 , and potential enhancer-hijacking events involving PIK3C3 and EPHA4, whose inhibition has shown therapeutic advantage in a number of cancer models [117][118][119]124 . Radke J, Ishaque N et al, Mutational landscape of PCNSL While the genetic landscape of PCNSL was described in some detail before [12][13][14]16,20,21,39,45,47 , studies investigating the global gene expression profile of PCNSL have been scarce so far.…”
Section: Discussionmentioning
confidence: 99%
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“…The landscape of copy number aberrations and structural variations revealed potentially clinically exploitable deletion of TOX as a predictor for anti-PD1 response 107 , amplification of MALT1, whose inhibition has been shown to be selectively toxic for ABC-DLBCL 152 , and potential enhancer-hijacking events involving PIK3C3 and EPHA4, whose inhibition has shown therapeutic advantage in a number of cancer models [117][118][119]124 . Radke J, Ishaque N et al, Mutational landscape of PCNSL While the genetic landscape of PCNSL was described in some detail before [12][13][14]16,20,21,39,45,47 , studies investigating the global gene expression profile of PCNSL have been scarce so far.…”
Section: Discussionmentioning
confidence: 99%
“…A number of other genes exhibited at least three times as many distal translocations (while still being the closest gene) than directly on the gene, including PIK3C3, EPHA4, SI, ALCAM, NCAM2, CADM2, CDH9, PABPC4L, GRIK2, POM121L12, ACO1, KLHL1, SLITRK1, and SLITRK6. Hyperactivation of PI3K signaling is one of the most common events in human cancers, and PIK3C3 has been shown to promote cell proliferation 115 and autophagy 116 , and its inhibition has shown therapeutic benefit in bladder, HCC and colon cancer [117][118][119] . EPHA4 has been described to promote cell proliferation and migration 120,121 and was associated with tumour aggressiveness and poor patient survival in human breast and rectal cancer 122,123 .…”
Section: Recurrent Structural Variations (Svs)mentioning
confidence: 99%
“…Singh et al synthesized 36-077, a specific and potent inhibitor of PIK3C3/VPS34 kinase. Co-treatment with 36-077 improves the efficacy of 5-FU, and suppressed GSK-3β/Wnt/β-catenin signaling to inhibit CSC population in HCT116 cells [118].…”
Section: Other Selective Pik3c3 Inhibitorsmentioning
confidence: 97%
“…Multiple studies have confirmed the essential role of PIK3C3/autophagy in the maintenance of CSCs. Autophagy-enriched HCT116 colon cancer cells induced by 5-FU treatment showed increased expression of CSC markers and 5-FU resistance [118]. Cotreatment with 36-077 (a PIK3C3 inhibitor) induced degradation of β-catenin protein with a reduction in the CSC population and significantly improved the efficacy of 5-FU treatment in HCT116 cells [118] (Figure 3).…”
Section: Cancer Stem Cells (Cscs)mentioning
confidence: 99%
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