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AKT

USP35, Regulated by Estrogen and AKT, Promotes Breast Tumorigenesis by Stabilizing and Enhancing Transcriptional Activity of Estrogen Receptor α

[Cell Death & Disease] USP35 promoted the growth of ER+ breast cancer in vitro and in vivo, and reduced the sensitivity of ER+ breast cancer cells to endocrine therapies such as tamoxifen and fulvestrant.

ISL1 Promoted Tumorigenesis and EMT via Aurora Kinase A-Induced Activation of PI3K/AKT Signaling Pathway in Neuroblastoma

[Cell Death & Disease] Investigators identified Insulin gene enhancer binding protein 1 (ISL1) as an oncogene in neuroblastoma (NB). ISL1 is preferentially upregulated in NB tissues compared with normal tissues.

Targeted PI3K/AKT-Hyperactivation Induces Cell Death in Chronic Lymphocytic Leukemia

[Nature Communications] Scientists hypothesized that targeted hyperactivation of the phosphatidylinositol-3-phosphate/AKT (PI3K/AKT)-signaling pathway may have been leveraged to trigger chronic lymphocytic leukemia cell death.

Cabozantinib Promotes Erythroid Differentiation in K562 Erythroleukemia Cells through Global Changes in Gene Expression and JNK Activation

[Cancer Gene Therapy] The authors reported that cabozantinib could promote differentiation in erythroid leukemia cells and found that K562 erythroid leukemia cells treated with 1 μM cabozantinib for 72 hours underwent erythroid lineage differentiation.

Depalmitoylation Rewires FLT3-ITD Signaling and Exacerbates Leukemia Progression

[Blood] Investigators discovered that FLT3-ITD, one of the most frequent mutations in acute myeloid leukemia, was S-palmitoylated by the ZDHHC6 palmitoyl acyltransferase. Disruption of palmitoylation redirected FLT3-ITD to the plasma membrane and rewired its downstream signaling by activating AKT and ERK pathways in addition to STAT5.

IMiDs Uniquely Synergize with TKIs to Upregulate Apoptosis of Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia Cells Expressing a Dominant-Negative IKZF1 Isoform

[Cell Death Discovery] Scientists found that lenalidomide, a representative of immunomodulatory drugs (IMiDs), specifically induced accumulation of Ik6 with the disappearance of functional isoforms within 24 hours in Ik6-positive Philadelphia chromosome-positive acute lymphoblastic leukemia cells in a neddylation-dependent manner.

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