journal
https://read.qxmd.com/read/35252555/g3bp1-modulates-spop-to-promote-prostate-tumorigenesis
#21
JOURNAL ARTICLE
Chandrani Mukhopadhyay, Pengbo Zhou
Speckle-type POZ protein (SPOP), a Cullin 3-based ubiquitin ligase (CUL3SPOP ), acts as a prostate-specific tumor suppressor. Loss-of-function mutations in SPOP occur in 10% of primary prostate cancer with a high Gleason grade and poor prognosis. However, it is unclear how the ubiquitin ligase activity of SPOP is controlled and how dysregulation of SPOP contributes to malignant transformation. Here, we identified GTPase Activating Protein (SH3 Domain) Binding Protein 1 (G3BP1) as an interactor and upstream regulator of CUL3SPOP , and it functions as an inhibitor of CUL3SPOP ubiquitin ligase, suggesting a distinctive mode of CUL3SPOP inactivation that aggravates prostate cancer...
2022: Molecular & Cellular Oncology
https://read.qxmd.com/read/35252554/escape-from-senescence-revisiting-cancer-therapeutic-strategies
#22
JOURNAL ARTICLE
Christos P Zampetidis, Argyris Papantonis, Vassilis G Gorgoulis
Although senescence has been considered as an irreversible cell arrest state, accumulating evidence challenge this view. Consequently, senescence appears as an imperfect barrier to impede cancer progression, constituting a step prior to disease relapse. Therefore, cancer treatment strategies may benefit if revisited to include senolytic agents.
2022: Molecular & Cellular Oncology
https://read.qxmd.com/read/35252553/resistance-to-kinase-inhibition-through-shortened-target-engagement
#23
JOURNAL ARTICLE
Aziz M Rangwala, Benedict-Tilman Berger, Matthew B Robers, Stefan Knapp, Markus A Seeliger
Imatinib, a selective inhibitor of the breakpoint cluster region (BCR)-ABL kinase, is the poster child for targeted cancer therapeutics. However, its efficacy is limited by resistance mutations. Using a quantitative bioluminescence resonance energy transfer assay in living cells, we identified ABL kinase mutations that could cause imatinib resistance by altering drug residence time.
2022: Molecular & Cellular Oncology
https://read.qxmd.com/read/35252552/barrett-s-esophagus-stages-their-correlation-with-sbs17-associated-dna-mutations-and-the-identification-of-histological-marker-genes
#24
JOURNAL ARTICLE
Georg A Busslinger
We have recently reported a correlation between the accumulation of specific T > C and T > G mutations and the chromosomal instability in cells of Barrett's esophagus (BE), which represents a premalignant condition of esophageal adenocarcinoma. Additionally, we identified seven marker genes that facilitate the distinction of individual BE stages by histopathological examination.
2022: Molecular & Cellular Oncology
https://read.qxmd.com/read/35252551/rewired-lipid-metabolism-as-an-actionable-vulnerability-of-aggressive-colorectal-carcinoma
#25
JOURNAL ARTICLE
Daria Capece, Guido Franzoso
Cancer cells reprogram lipid metabolism to fuel cell division, adaptation to stress, and metastatic dissemination. NF-κB transcription factors control this mechanism in aggressive Consensus Molecular Subtype (CMS)4 of colorectal carcinoma (CRC) via triacylglycerol (TAG) lipase, carboxylesterase 1 (CES1), thereby linking obesity-associated inflammation with metabolic adaptation and cytoprotection from lipid-induced toxicity. Our findings identify a potential therapeutic route to treat patients with metastasis-prone CRC and provide an example for targeting core tumor subtype-based vulnerabilities in cancers beyond CRC...
2022: Molecular & Cellular Oncology
https://read.qxmd.com/read/35252550/tumor-suppressor-pathways-shape-egfr-driven-lung-tumor-progression-and-response-to-treatment
#26
JOURNAL ARTICLE
Giorgia Foggetti, Chuan Li, Hongchen Cai, Dmitri A Petrov, Monte M Winslow, Katerina Politi
In vivo modeling combined with CRISPR/Cas9-mediated somatic genome editing has contributed to elucidating the functional importance of specific genetic alterations in human tumors. Our recent work uncovered tumor suppressor pathways that affect EGFR-driven lung tumor growth and sensitivity to tyrosine kinase inhibitors and reflect the mutational landscape and treatment outcomes in the human disease.
2022: Molecular & Cellular Oncology
https://read.qxmd.com/read/34027048/hdac2-links-ubiquitination-to-tumor-suppression-in-synovial-sarcoma
#27
JOURNAL ARTICLE
Christina Cooley, Le Su
The function of histone deacetylase 2 (HDAC2) in transcriptional regulation and its role in oncogenesis have been well established. Here we discuss a transcription-independent HDAC2 pathway controlling cancer-related protein stability via the mouse double minute 2 homolog (MDM2) ubiquitin ligase. In synovial sarcoma, HDAC2 inactivation demonstrates significant therapeutic effect by degradation of the SS18-SSX driver oncoprotein.
April 25, 2021: Molecular & Cellular Oncology
https://read.qxmd.com/read/34027044/new-link-between-the-rna-polymerase-ii-ctd-and-replication-stress
#28
JOURNAL ARTICLE
Helga B Landsverk, Lise E Sandquist, Lilli T E Bay, Randi G Syljuåsen
Conflicts between transcription and replication are a major source of replication stress. Our recent findings show that proper dephosphorylation of Serine 5 in the carboxy-terminal domain (CTD) of DNA-directed RNA polymerase II subunit RPB1 is needed to prevent such conflicts in human cells.
April 18, 2021: Molecular & Cellular Oncology
https://read.qxmd.com/read/34027038/the-complex-role-of-sirt7-in-p53-stabilization-nucleophosmin-joins-the-debate
#29
JOURNAL ARTICLE
Poonam Kumari, Shahriar Tarighi, Thomas Braun, Alessandro Ianni
Release of nucleophosmin (NPM) from nucleoli following stress promotes rapid stabilization of the tumor suppressor p53 (TP53, best known as p53). Nucleoplasmic NPM binds to the ubiquitin ligase mouse double minute 2 (MDM2) and prevents MDM2-dependent p53 degradation. We recently demonstrated that sirtuin 7 (SIRT7) activates this pathway by directly deacetylating NPM following ultraviolet irradiation, indicating tumor-suppressive functions of SIRT7.
March 31, 2021: Molecular & Cellular Oncology
https://read.qxmd.com/read/34027041/targeting-one-carbon-metabolism-requires-mtor-inhibition-a-new-therapeutic-approach-in-osteosarcoma
#30
JOURNAL ARTICLE
Richa Rathore, Brian Van Tine
The rate-limiting enzyme of serine biosynthesis, 3-phosphoglycerate dehydrogenase (PHGDH), contributes to rapid growth and proliferation when it is overexpressed in cancer. We recently described the metabolic adaptations that occur upon PHGDH inhibition in osteosarcoma. PHGDH inhibition causes metabolite accumulation that activates the mechanistic target of rapamycin (mTOR) signaling, sensitizing osteosarcoma to non-rapalog mTOR inhibition.
March 25, 2021: Molecular & Cellular Oncology
https://read.qxmd.com/read/33855170/p62-sqstm1-droplets-initiate-autophagosome-biogenesis-and-oxidative-stress-control
#31
JOURNAL ARTICLE
Eeva-Liisa Eskelinen, Shun Kageyama, Masaaki Komatsu
Selective autophagy contributes to the degradation of condensates, such as sequestosome 1-bodies, also called p62/SQSTM1-bodies. We showed that endogenous p62 forms gel-like structures, which serve as platforms for autophagosome formation and nuclear factor erythroid 2-related factor 2 (NRF2) activation. Further, p62-mediated NRF2 activation is not cytotoxic, but combination of NRF2 activation with impaired bulk and selective autophagy causes liver injury.
March 9, 2021: Molecular & Cellular Oncology
https://read.qxmd.com/read/33855165/control-of-s-phase-duration-a-replication-capacity-model-with-e2f-transcription-at-its-heart
#32
JOURNAL ARTICLE
Cosetta Bertoli, Robertus A M de Bruin
DNA replication capacity, the maximal amount of DNA a cell can synthesize at any given time during S phase, is controlled by E2F-dependent transcription. Controlling replication capacity limits the replication rate and provides a robust mechanism to keep replication fork speed within an optimal range whilst ensuring timely completion of genome duplication.
March 8, 2021: Molecular & Cellular Oncology
https://read.qxmd.com/read/33855169/tuning-protein-synthesis-for-cancer-therapy
#33
JOURNAL ARTICLE
John R P Knight, Owen J Sansom
~50% of colorectal cancers have an activating mutation in KRAS (encoding the KRAS proto-oncogene) and remain difficult to target in the clinic. We have recently shown that activation of KRAS protein alters the regulation of mRNA translation, increasing total protein synthesis, and maintaining elevated c-MYC (MYC proto-oncogene) expression. Targeting these pathways downstream of KRAS reveals a striking dependency that has potential for clinical translation.
February 22, 2021: Molecular & Cellular Oncology
https://read.qxmd.com/read/33855168/mechanical-softness-a-true-stemness-feature-for-cancer-cells
#34
JOURNAL ARTICLE
Jiadi Lv, Yuying Liu, Bo Huang
Developing a method that can effectively define and sort cancer stem cells (CSCs) is extremely desirable. Mechanical stiffness is of paramount importance for a cell to differentiate and can reflect the differentiation state of cells. In line with this notion, cell softness is identified to be a unique marker for highly tumorigenic CSCs.
February 16, 2021: Molecular & Cellular Oncology
https://read.qxmd.com/read/33855166/targeting-gliomas-with-stat3-silencing-nanoparticles
#35
JOURNAL ARTICLE
Padma Kadiyala, Jason V Gregory, Pedro R Lowenstein, Joerg Lahann, Maria G Castro
Glioblastoma is an aggressive brain tumor with poor prognosis. The brain is protected by the blood-brain barrier, which precludes transport of chemotherapeutics. We developed nanoparticles that achieve delivery of small-interfering RNA against Stat3 after systemic administration. Nanoparticles combined with radiation inhibited tumor progression and elicited anti-glioblastoma immunity in mice.
January 31, 2021: Molecular & Cellular Oncology
https://read.qxmd.com/read/33855167/a-jak-of-all-trades-how-global-phosphoproteomics-reveal-the-achilles-heel-of-mpns
#36
JOURNAL ARTICLE
Tina M Schnoeder, Florian Perner, Florian H Heidel
While Janus-kinase (JAK)-inhibitors effectively reduce the inflammatory phenotype of myeloproliferative neoplasms (MPN), they do not affect disease burden or presence of the mutated clone to a major extent. Here, we show how Janus-kinase 2 ( JAK2) -mutated cells persist through maintenance of the mitogen-activated protein kinase Interacting Serine/Threonine Kinase 1 (MKNK1) - Extracellular Signal-regulated Kinase (ERK)-axis by hijacking the splicing machinery through post-translational modifications.
January 30, 2021: Molecular & Cellular Oncology
https://read.qxmd.com/read/33553613/src-promotes-lipogenesis-implications-for-obesity-and-breast-cancer
#37
JOURNAL ARTICLE
Shu-Yong Lin, Sheng-Cai Lin
Remodeling of lipid metabolism has been implicated in cancers; however, it remains obscure how the lipid metabolic pathways are altered by oncogenic signaling to affect tumor development. We have recently shown that proto-oncogene tyrosine-protein kinase Src interacts with and phosphorylates the lipogenesis enzyme phosphatidate phosphatase LPIN1 to promote breast cancer development.
January 12, 2021: Molecular & Cellular Oncology
https://read.qxmd.com/read/33553610/bok-mcl1-transmembrane-interactions-a-challenging-target-for-cancer-therapy
#38
JOURNAL ARTICLE
Mónica Sancho, Mar Orzáez
Myeloid cell leukemia 1 ( MCL1 ) gene amplification occurs in a wide range of human cancers and protein overexpression associates with malignant cell growth and evasion of apoptosis. We recently reported that disrupting the interaction between the transmembrane domains of MCL1 and BCL-2 related ovarian killer (BOK) induces cell death, thereby suggesting a new target site for anti-tumorigenic strategies.
January 11, 2021: Molecular & Cellular Oncology
https://read.qxmd.com/read/33553605/the-senescence-associated-secretory-phenotype-as-a-driver-of-tumor-growth-does-g3bp1-hold-the-key
#39
JOURNAL ARTICLE
Amr Omer, Sergio Di Marco, Imed-Eddine Gallouzi
Cellular senescence is a double-edged sword that, depending on the context, acts as either a potent tumor protective mechanism or an age-related driver of diseases such as cancer. Our recent findings show that the rasGAP SH3-binding protein 1 (G3BP1) activates the senescent-associated secretory phenotype (SASP) that, in turn, mediates cancer growth/progression.
January 11, 2021: Molecular & Cellular Oncology
https://read.qxmd.com/read/33553609/targeting-ganglioneuromas-with-mtor-inhibitors
#40
JOURNAL ARTICLE
Ting Tao, Hui Shi, Adam D Durbin, A Thomas Look
We recently identified activated protein kinase B (PKB/AKT) as a tumorigenic driver in childhood ganglioneuroma. Inhibition of the mechanistic target of rapamycin (mTOR), a serine/threonine kinase downstream of AKT, effectively reduced the tumor burden in zebrafish with ganglioneuroma. We propose a clinical trial of mTOR inhibitors as a means to shrink large ganglioneuromas prior to surgical resection.
January 10, 2021: Molecular & Cellular Oncology
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