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Hydrogen sulfide operates as a glioblastoma suppressor and is lost under high fat diet. 硫化氢是一种胶质母细胞瘤抑制剂，在高脂肪饮食中会减少。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-09-16 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1973312
Daniel J Silver, Justin D Lathia, Christopher Hine
{"title":"Hydrogen sulfide operates as a glioblastoma suppressor and is lost under high fat diet.","authors":"Daniel J Silver,&nbsp;Justin D Lathia,&nbsp;Christopher Hine","doi":"10.1080/23723556.2021.1973312","DOIUrl":"https://doi.org/10.1080/23723556.2021.1973312","url":null,"abstract":"<p><p>Glioblastoma (GBM) is one of the deadliest and aggressive forms of brain cancer. Environmental and intrinsic factors such as Western Diet and advanced age can function as powerful accelerants to the progression of GBM. Recently, we discovered that pre-clinical GBM models subject to an obesogenic and age-accelerating high fat diet (HFD) presented with hyperaggressive GBM phenotypes, including treatment-refractory cancer stem cell (CSC) enrichment. Mechanistically, HFD suppressed production of the gasotransmitter hydrogen sulfide (H<sub>2</sub>S) and its downstream sulfhydration signaling in the brain. Likewise, we observed dramatic loss of sulfhydration in brains of GBM patients. Importantly, we showed the tumor suppressive effects of H<sub>2</sub>S against GBM in cell culture and <i>in vivo</i>. Here, we discuss these recent findings and provide insight into how they can be leveraged to improve treatment modalities, prognosis, and quality of life for GBM patients.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 4","pages":"1973312"},"PeriodicalIF":2.1,"publicationDate":"2021-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8489903/pdf/KMCO_8_1973312.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39491986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A late endosome signaling hub that couples PI3Kα and WNT/β-catenin signaling in breast cancer. 在乳腺癌中偶联PI3Kα和WNT/β-catenin信号的晚期核内体信号中枢。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-09-09 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1954470
Samuel J Rodgers, Sabryn A Hamila, Christina A Mitchell, Lisa M Ooms
{"title":"A late endosome signaling hub that couples PI3Kα and WNT/β-catenin signaling in breast cancer.","authors":"Samuel J Rodgers,&nbsp;Sabryn A Hamila,&nbsp;Christina A Mitchell,&nbsp;Lisa M Ooms","doi":"10.1080/23723556.2021.1954470","DOIUrl":"https://doi.org/10.1080/23723556.2021.1954470","url":null,"abstract":"<p><p>AKT is the central phosphoinositide 3-kinase (PI3K) signaling effector, however, <i>PIK3CA</i> (p110α subunit of PI3Kα)-mutant estrogen receptor-positive (ER<sup>+</sup>) breast cancers exhibit minimal AKT activation and the downstream signaling is poorly characterized. We discovered that a subset of <i>PIK3CA</i>-mutant ER<sup>+</sup> breast cancers exhibit increased inositol polyphosphate 4-phosphatase type II (INPP4B) expression, which promotes late endosome formation and glycogen synthase kinase 3 beta (GSK3β) trafficking, leading to enhanced Wingless-related integration site (WNT)/catenin beta 1 (β-catenin) activation.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 4","pages":"1954470"},"PeriodicalIF":2.1,"publicationDate":"2021-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8489923/pdf/KMCO_8_1954470.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39491985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Predicting survival of cancer patients by chromosomal copy number heterogeneity. 通过染色体拷贝数异质性预测癌症患者的生存。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-08-03 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1949956
Tom Van Den Bosch, Erik van Dijk, Louis Vermeulen, Daniël M Miedema
{"title":"Predicting survival of cancer patients by chromosomal copy number heterogeneity.","authors":"Tom Van Den Bosch,&nbsp;Erik van Dijk,&nbsp;Louis Vermeulen,&nbsp;Daniël M Miedema","doi":"10.1080/23723556.2021.1949956","DOIUrl":"https://doi.org/10.1080/23723556.2021.1949956","url":null,"abstract":"ABSTRACT We recently introduced a method to derive intra-tumor heterogeneity (ITH) from a single copy number measurement. This method stratifies patients for survival and could potentially help to identify low and high-risk patients with clinical relevance.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 4","pages":"1949956"},"PeriodicalIF":2.1,"publicationDate":"2021-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1949956","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39491984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
BNIP3 in melanoma: isn't it IRONic? 黑色素瘤中的BNIP3:这不是很讽刺吗?
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-08-02 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1947169
Mónica Vara-Pérez, Patrizia Agostinis
{"title":"BNIP3 in melanoma: isn't it IRONic?","authors":"Mónica Vara-Pérez,&nbsp;Patrizia Agostinis","doi":"10.1080/23723556.2021.1947169","DOIUrl":"https://doi.org/10.1080/23723556.2021.1947169","url":null,"abstract":"<p><p>Melanoma cells exploit mitophagy and hypoxia signaling to promote their growth. In a recent study, we found that loss of B-cell lymphoma 2 (BCL-2)/adenovirus E1B 19kDa protein-interacting protein 3 (BNIP3) curbed Hypoxia Inducible Factor 1 alpha (HIF-1α) levels and melanoma growth <i>in vivo</i>. Insufficient levels of BNIP3 boost iron-driven prolyl hydroxylase 2 (Phd2)-mediated degradation of HIF-1α by exacerbating nuclear receptor activator 4 (Ncoa4)-mediated ferritinophagy. Thus, BNIP3 promotes melanoma growth by controlling iron metabolism.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 4","pages":"1947169"},"PeriodicalIF":2.1,"publicationDate":"2021-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8489953/pdf/KMCO_8_1947169.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39492060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
AMBRA1 and FAK1: crosstalking for improved targeted therapy in melanoma. AMBRA1和FAK1:串扰改善黑色素瘤靶向治疗。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-07-13 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1949955
Luca Di Leo, Daniela De Zio
{"title":"AMBRA1 and FAK1: crosstalking for improved targeted therapy in melanoma.","authors":"Luca Di Leo,&nbsp;Daniela De Zio","doi":"10.1080/23723556.2021.1949955","DOIUrl":"https://doi.org/10.1080/23723556.2021.1949955","url":null,"abstract":"<p><p>Through genetically engineered mouse models of melanoma, we identified Autophagy/beclin 1 regulator 1 (Ambra1) as novel tumor-suppressor in melanoma. In these settings, loss of <i>Ambra1</i> associated with the hyperactivation of focal adhesion kinase 1 (Fak1) signaling, the inhibition of which resulted in reduced tumor growth and invasiveness. We therefore propose FAK1 inhibition for current melanoma therapy in AMBRA1-low tumors.</p><p><strong>Abbreviations: </strong>AKT, serine/threonine kinase 1; AMBRA1, autophagy/beclin 1 regulator 1; BRAF, v-raf murine sarcoma viral oncogene homolog; BRAFi, BRAF inhibitor; CCLE, Cancer Cell Line Encyclopedia;g ESTDAB, European Searchable Tumor Line Database; FAK1, focal adhesion kinase 1; FAKi, FAK1 inhibitor; LMC, Leeds Melanoma Cohort; MEK, MAPK/ERK kinase; PP2A, protein phosphatase 2A; PTEN, phosphatase and tensin homolog; TCGA-SKCM, The Cancer Genome Atlas - Skin Cutaneous Melanoma; YAP, yes-associated protein 1.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 4","pages":"1949955"},"PeriodicalIF":2.1,"publicationDate":"2021-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1949955","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39491983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
TFG: a novel regulator of ULK1-dependent autophagy. TFG:一种新的ulk1依赖性自噬调节因子。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-07-12 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1945895
Francesco Cecconi, Francesca Nazio
{"title":"TFG: a novel regulator of ULK1-dependent autophagy.","authors":"Francesco Cecconi,&nbsp;Francesca Nazio","doi":"10.1080/23723556.2021.1945895","DOIUrl":"https://doi.org/10.1080/23723556.2021.1945895","url":null,"abstract":"<p><p>TRK-fused gene (TFG) is a protein implicated in multiple neurodegenerative diseases and oncogenesis. We have recently shown that, under starvation conditions, TFG contributes to spatial control of autophagy by facilitating Unc-51 like autophagy activating kinase 1 (ULK1)-microtubule-associated protein 1 light chain 3 gamma (MAP1LC3C) interaction to modulate omegasome and autophagosome formation. Defective TFG-mediated autophagy could thus be postulated as a possible contributor to ontogenesis or progression of TFG-related diseases.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 4","pages":"1945895"},"PeriodicalIF":2.1,"publicationDate":"2021-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1945895","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39492059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Non-neuroendocrine differentiation generates a ferroptosis-prone lipidome in small cell lung cancer (SCLC). 在小细胞肺癌(SCLC)中，非神经内分泌分化产生一个易致铁凋亡的脂质组。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-07-05 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1933871
Christina M Bebber, Silvia von Karstedt
{"title":"Non-neuroendocrine differentiation generates a ferroptosis-prone lipidome in small cell lung cancer (SCLC).","authors":"Christina M Bebber,&nbsp;Silvia von Karstedt","doi":"10.1080/23723556.2021.1933871","DOIUrl":"https://doi.org/10.1080/23723556.2021.1933871","url":null,"abstract":"<p><p>Our recent study revealed that non-neuroendocrine small cell lung cancer (SCLC) is sensitive to the induction of ferroptosis due to upregulation of ether lipid synthesis. While neuroendocrine SCLC is ferroptosis resistant, it acquires addiction to the thioredoxin pathway. Combined redox pathway targeting therefore achieves efficient anti-tumor activity in heterogenous SCLC.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 4","pages":"1933871"},"PeriodicalIF":2.1,"publicationDate":"2021-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1933871","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39492056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
Cancer-associated keratinocytes: new members of the microenvironment in head and neck cancer. 癌症相关角化细胞:头颈癌微环境的新成员
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-07-01 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1933329
Erika B Danella, Marcell Costa De Medeiros, Nisha J D'Silva
{"title":"Cancer-associated keratinocytes: new members of the microenvironment in head and neck cancer.","authors":"Erika B Danella,&nbsp;Marcell Costa De Medeiros,&nbsp;Nisha J D'Silva","doi":"10.1080/23723556.2021.1933329","DOIUrl":"https://doi.org/10.1080/23723556.2021.1933329","url":null,"abstract":"<p><p>The tumor microenvironment is a complex ecosystem of malignant and nonmalignant cells and extracellular proteins that work together to enhance tumor progression. We identified a mechanism in which adjacent nonmalignant epithelium enhances invasion of squamous cell carcinoma, thereby expanding the tumor microenvironment to include cancer-associated keratinocytes.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 4","pages":"1933329"},"PeriodicalIF":2.1,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1933329","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39492055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
A direct role of RNA polymerase III and RNA in DNA homologous recombination. RNA聚合酶III和RNA在DNA同源重组中的直接作用。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-07-01 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1935173
Sijie Liu, Daochun Kong
{"title":"A direct role of RNA polymerase III and RNA in DNA homologous recombination.","authors":"Sijie Liu,&nbsp;Daochun Kong","doi":"10.1080/23723556.2021.1935173","DOIUrl":"https://doi.org/10.1080/23723556.2021.1935173","url":null,"abstract":"<p><p>End resection excises several thousand bases from the 5'-ended strand during DNA double-strand break repair, creating 3'-end single-stranded DNA overhangs. This overhang requires strict protection from DNA2 or other nucleases digestion. A recent finding showed that the 3'-end overhangs are protected by the transient formation of RNA-DNA hybrids, and RNA polymerase III is an essential factor for homologous recombination.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 4","pages":"1935173"},"PeriodicalIF":2.1,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1935173","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39492057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
Novel subtypes of NPM1-mutated AML with distinct outcome. 具有不同结果的npm1突变AML的新亚型。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-06-30 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1924600
Arvind Singh Mer, Mark D Minden, Benjamin Haibe-Kains, Aaron D Schimmer
{"title":"Novel subtypes of <i>NPM1</i>-mutated AML with distinct outcome.","authors":"Arvind Singh Mer,&nbsp;Mark D Minden,&nbsp;Benjamin Haibe-Kains,&nbsp;Aaron D Schimmer","doi":"10.1080/23723556.2021.1924600","DOIUrl":"https://doi.org/10.1080/23723556.2021.1924600","url":null,"abstract":"<p><p>Acute myeloid leukemia (AML) is heterogeneous with one common subtype recognized by the presence of recurrent mutation of nucleophosmin-1 (<i>NPM1</i>). Emerging evidence indicates that within <i>NPM1</i> mutated AML there is variation in outcome which challenges how best to characterize and treat the individual patient. Our recent findings show that there are two distinct (primitive and committed) subtypes within <i>NPM1</i> mutated AML patients. These subtypes exhibit specific molecular characteristics, disease differentiation states, patient survival, and differential drug responses.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 4","pages":"1924600"},"PeriodicalIF":2.1,"publicationDate":"2021-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1924600","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39492053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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