Polypyrimidine tract-binding protein 1-mediated down-regulation of ATG10 facilitates metastasis of colorectal cancer cells

Jo, Yoon Kyung; Roh, Seon Ae; Lee, Heejin; Park, Na Yeon; Choi, Eun Sun; Oh, Ju‐Hee; Park, Soo‐Young; Shin, Ji Hyun; Suh, Young‐Ah; Lee, Eun Kyung; Cho, Dong‐Hyung; Kim, Jin Cheon

doi:10.1016/j.canlet.2016.11.002

Cited by 58 publications

(48 citation statements)

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“…46 A previous study reported that increased ATG10 expression was strongly associated with tumor invasion and metastasis, and, as an oncogenic gene, ATG10 may be a potential prognostic maker for colorectal cancer. 31 In one study of 1064 breast cancer cases and 1073 cancer-free controls in a Chinese population, the authors found that genetic variants in ATG10 rs10514231 were associated with risk of breast cancer. 30 More recently, in another survival study of 1001 Chinese NSCLC patients, Xie et al observed that variant alleles of rs10514231 and rs1864182 were associated with a poor overall survival, and these variants were associated with the increased methylation levels of cg17942617.…”

Section: Discussionmentioning

confidence: 99%

“…The selection of candidate genes ATGB2 , 17, 29 ATG10 , 8, 30, 31 ATG12 21, 32, 33 and ATG16L2 34-36 was based on previously published studies, which show a positive association with risk of diseases including cancers. Using the public HapMap SNP database (phase II + III, August10, on NCBI B36 assembly, dbSNP b126) and the HaploView 4.2 software, common SNPs [a minor allele frequency (MAF) ≥ 0.05] in ATG2B, ATG10, ATG12 , and ATG16L2 were screened for in their gene regions (within these genes or ± 2-kb flanking regions) in CEU populations.…”

Section: Methodsmentioning

confidence: 99%

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Potentially Functional Variants of ATG16L2 Predict Radiation Pneumonitis and Outcomes in Patients with Non–Small Cell Lung Cancer after Definitive Radiotherapy

Jiang

Liu

Wang

et al. 2018

Journal of Thoracic Oncology

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Introduction: Autophagy not only plays an important role in the progression of cancer but also is involved in tissue inflammatory response. However, few published studies have investigated associations between functional genetic variants of autophagy-related genes and radiation pneumonitis (RP) as well as clinical outcomes in patients with non-small cell lung cancer (NSCLC) after definitive radiotherapy. Methods: We genotyped nine potentially functional single nucleotide polymorphisms (SNPs) in four autophagy-related genes (ATG2B, ATG10, ATG12 and ATG16L2) in 393 NSCLC patients of a North American population and assessed their association with RP, local recurrence-free survival (LRFS), progression-free survival (PFS) and overall survival (OS) in multivariate Cox proportional hazards regression analyses. These patients had NSCLC that was treated by definitive radiotherapy. Results: We found that the ATG16L2 rs10898880 CC variant homozygotes had a better LRFS, PFS and OS [adjusted hazards ratio (adjHR) = 0.59, 0.64 and 0.64; 95% confidence interval (95% CI = 0.45-0.79, 0.54-0.96, 0.48-0.84, and 0.48-0.86); and P = 0.0004, 0.002, and 0.003, respectively], but a greater risk of developing severe RP, than patients with CC/CT genotypes (adjHR = 1.80, 96% CI = 1.04-3.12, P = 0.037). Further functional analyses suggested that the ATG16L2 rs10898880 C variant allele modulated gene expression of ATG16L2. Conclusion: This is the first report that functional ATG16L2 C variant homozygous genotype may be a predictor of RP, LRFS, PFS, and OS in NSCLC patients after definitive radiotherapy. Additional larger, prospective studies are needed to confirm these findings.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Potentially Functional Variants of ATG16L2 Predict Radiation Pneumonitis and Outcomes in Patients with Non–Small Cell Lung Cancer after Definitive Radiotherapy

Jiang

Liu

Wang

et al. 2018

Journal of Thoracic Oncology

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“…It was previously reported that overexpression of Beclin-1 in vitro inhibited CRC cells growth and enhanced the rapamycin-induced antitumor effects (136). Patients with high levels of Beclin-1 presented good prognosis and longer survival (131, 135), and ATG10 downregulation was associated with cell migration and invasion of CRC cells (137). In addition, several compounds were recently demonstrated to suppress colorectal carcinogenesis through the induction of autophagy, including Salvianolic acid B and IR-58 (138, 139).…”

Section: The Roles Of Autophagy In Ibdmentioning

confidence: 99%

Intestinal Autophagy and Its Pharmacological Control in Inflammatory Bowel Disease

Peng

Shao

et al. 2017

Front. Immunol.

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Intestinal mucosal barrier, mainly composed of the intestinal mucus layer and the epithelium, plays a critical role in nutrient absorption as well as protection from pathogenic microorganisms. It is widely acknowledged that the damage of intestinal mucosal barrier or the disturbance of microorganism balance in the intestinal tract contributes greatly to the pathogenesis and progression of inflammatory bowel disease (IBD), which mainly includes Crohn’s disease and ulcerative colitis. Autophagy is an evolutionarily conserved catabolic process that involves degradation of protein aggregates and damaged organelles for recycling. The roles of autophagy in the pathogenesis and progression of IBD have been increasingly studied. This present review mainly describes the roles of autophagy of Paneth cells, macrophages, and goblet cells in IBD, and finally, several potential therapeutic strategies for IBD taking advantage of autophagy.

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“…Previously, the role of autophagy in cancer therapy has been proposed. It is now well accepted that in response to various chemotherapeutic drugs, radiation, and targeted therapeutics, cancer cells show large‐scale accumulation of autophagic vacuoles . It has been reported that TAM induces autophagy in tumor cells .…”

Section: Discussionmentioning

confidence: 99%

“…It is now well accepted that in response to various chemotherapeutic drugs, radiation, and targeted therapeutics, cancer cells show large-scale accumulation of autophagic vacuoles. [39][40][41] It has been reported that TAM induces autophagy in tumor cells. 26,42 Herein, Figure 3 showed that TAM increased autolysosome and the ratio of LC3II/LC3I mainly in U87 cells while potently inducing apoptosis in U251 cells.…”

Section: Discussionmentioning

confidence: 99%

Estrogen receptor variant ER‐α36 promotes tamoxifen agonist activity in glioblastoma cells

Zhang

et al. 2019

Cancer Science

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Glioblastoma (GBM) is a highly infiltrative and malignant primary brain tumor. Despite aggressive therapy, patients with GBM have a dismal prognosis with median survival of approximately 1 year. Tamoxifen (TAM), a selective estrogen receptor modulator (SERM), has been used to treat GBM for many years. ER‐α36 is a novel variant of estrogen receptor‐alpha66 (ER‐α66) and can mediate cell proliferation through estrogen or anti‐estrogen signaling in different cancer cells. Previously, we found that ER‐α36 was highly expressed in GBM and was involved in the tamoxifen sensitivity of glioblastoma cells. However, the molecular mechanism responsible has not been well established. Here, we found that ER‐α36 is highly expressed in glioblastoma specimens. We further found that ER‐α36 knockdown increased sensitivity of glioblastoma U87 cells to TAM and decreased autophagy in these cells. However, ER‐α36 overexpression decreased TAM sensitivity and induced autophagy. We also established TAM‐resistant glioblastoma U251 cells by a long‐term culture in TAM‐containing medium and found that TAM‐resistant cells showed a six‐fold increase of ER‐α36 mRNA expression and elevated basal autophagy. ER‐α36 knockdown in these TAM‐resistant cells restored TAM sensitivity. In addition, we recapitulated the physiologically relevant tumor microenvironment in an integrated microfluidic device, and U87 cells were treated with a gradient of TAM. We found that ER‐α36 expression is consistent with autophagy protein P62 in a three‐dimensional microenvironment. In summary, these results indicate that ER‐α36 contributes to tamoxifen resistance in glioblastoma cells presumably through regulation of autophagy.

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Polypyrimidine tract-binding protein 1-mediated down-regulation of ATG10 facilitates metastasis of colorectal cancer cells

Cited by 58 publications

References 45 publications

Potentially Functional Variants of ATG16L2 Predict Radiation Pneumonitis and Outcomes in Patients with Non–Small Cell Lung Cancer after Definitive Radiotherapy

Potentially Functional Variants of ATG16L2 Predict Radiation Pneumonitis and Outcomes in Patients with Non–Small Cell Lung Cancer after Definitive Radiotherapy

Intestinal Autophagy and Its Pharmacological Control in Inflammatory Bowel Disease

Estrogen receptor variant ER‐α36 promotes tamoxifen agonist activity in glioblastoma cells

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