ALKBH1 drives tumorigenesis and drug resistance via tRNA decoding reprogramming and codon-biased translation.

Cancer cells utilize codon-biased translation to fuel tumorigenesis and drug resistance, but underlying mechanisms remain poorly understood. Here, we show ALKBH1 is overexpressed in acute myeloid leukemia (AML) and essential for leukemia stem/initiating cell (LSC/LIC) self-renewal and AML development/maintenance, whereas dispensable for normal hematopoiesis. ALKBH1 enhances mitochondrial assembly/function and oxidative phosphorylation (OXPHOS), crucial for AML survival/proliferation and resistance to venetoclax, a potent BCL2 inhibitor and widely-used first-line targeted therapy for AML in clinic.

PSPH promotes the proliferation and metastasis of esophageal squamous cell carcinoma through MAPK signaling pathways.

Esophageal squamous cell carcinoma (ESCC) is an aggressive malignancy with limited therapeutic options and poor prognosis, underscoring the urgent need for novel molecular targets. Here, we identify phosphoserine phosphatase (PSPH) as a key oncogenic driver in ESCC. This study systematically investigated the oncogenic functions of PSPH in ESCC progression and the associated molecular mechanisms.

PAXIP1 is regulated by NRF1 and is a prognosis‑related biomarker in hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is characterized by a poor prognosis globally. PAX-interacting protein 1 (PAXIP1) serves a key role in the development of numerous human cancer types. Nevertheless, its specific involvement in HCC remains poorly understood.

Harnessing m1A modification: a new frontier in cancer immunotherapy.

N1-methyladenosine (m1A) modification is an epigenetic change that occurs on RNA molecules, regulated by a suite of enzymes including methyltransferases (writers), demethylases (erasers), and m1A-recognizing proteins (readers). This modification significantly impacts the function of RNA and various biological processes by affecting the structure, stability, translation, metabolism, and gene expression of RNA. Thereby, m1A modification is closely associated with the occurrence and progression of cancer.

RBM15 increase tumor-infiltrating CD4+ T cell in ESCC modulating of PLOD3.

Background: Collagen, a primary protein component of the extracellular matrix (ECM), undergoes a notable series of alterations concomitant with the growth of the tumor. Procollagen-lysine,2-oxoglutarate 5-dioxygenase 3 (PLOD3) is involved in the synthesis of collagen and has been associated with a variety of cancers. However, it is unclear how PLOD3 functions in esophageal squamous cell carcinoma (ESCC).

Anti-reflux effects of a novel esophagogastric asymmetric anastomosis technique after laparoscopic proximal gastrectomy.

Background: Reflux esophagitis is a common postoperative complication of proximal gastrectomy. There is an urgent need for a safer method of performing esophageal-gastric anastomosis that reduces the risk of reflux after proximal gastrectomy. We hypothesize that a novel technique termed esophagogastric asymmetric anastomosis (EGAA) can prevent postoperative reflux in a safe and feasible manner.

[Transcriptome Analysis of Chronic Myelogenous Leukemia Cell Line with Imatinib Resistance].

Objective: To investigate the regulation of chronic myelogenous leukemia （CML） imatinib resistant genes, in order to improve the therapeutic effect of CML imatinib resistant patients.

Methods: The human CML cell line K562 and imatinib-resistant K562 cells (K562/G01) were collected, and transcriptome of the cells were achieved by RNA-seq. The sequencing data were analyzed by using standard procedures.

An Aggregation-Free Local Volume Fraction Formulation for Topological Design of Porous Structure.

Cellular structure can possess superior mechanical properties and low density simultaneously. Additive manufacturing has experienced substantial progress in the past decades, which promotes the popularity of such bone-like structure. This paper proposes a methodology on the topological design of porous structure.

PTIP Inhibits Cell Invasion in Esophageal Squamous Cell Carcinoma Modulation of EphA2 Expression.

Esophageal squamous cell carcinoma (ESCC) is a highly aggressive malignancy and treatment failure is largely due to metastasis and invasion. Aberrant tumor cell adhesion is often associated with tumor progression and metastasis. However, the exact details of cell adhesion in ESCC progression have yet to be determined.

KDM6A promotes imatinib resistance through YY1-mediated transcriptional upregulation of TRKA independently of its demethylase activity in chronic myelogenous leukemia.

Despite landmark therapy of chronic myelogenous leukemia (CML) with tyrosine kinase inhibitors (TKIs), drug resistance remains problematic. Cancer pathogenesis involves epigenetic dysregulation and in particular, histone lysine demethylases (KDMs) have been implicated in TKI resistance. We sought to identify KDMs with altered expression in CML and define their contribution to imatinib resistance.

LZ-106, a potent lysosomotropic agent, causing TFEB-dependent cytoplasmic vacuolization.

Cytoplasmic vacuolization usually occurs in cells treated with different agents and substances. We found that LZ-106, an analog of enoxacin, is a potent lysosomotropic agent, contributing to the formation of cytoplasmic vacuoles in cells. Studies of LZ-106-induced vacuolization in H460 cells showed acid environment inside these vacuoles.

G1 phase cell cycle arrest in NSCLC in response to LZ-106, an analog of enoxacin, is orchestrated through ROS overproduction in a P53-dependent manner.

LZ-106, a newly synthetized analog of quinolone, has been shown to be highly effective in non-small cell lung cancer (NSCLC) in both cultured cells and xenograft mouse model with low toxicity, yet the molecular mechanisms still require exploration. Here, we substantiated the involvement of P53 activation in intracellular reactive oxygen species (ROS) generation upon LZ-106 treatment and related P53 to the ROS-induced viability inhibition and apoptosis, which was exhibited in the previous research. P53 was shown to play an indispensable role in the elevated levels of intracellular ROS in LZ-106-treated NSCLC cells through ROS detection.

BRCA mutations and survival in breast cancer: an updated systematic review and meta-analysis.

BRCA mutations occur frequently in breast cancer (BC), but their prognostic impact on outcomes of BC has not been determined. We conducted an updated meta-analysis on the association between BRCA mutations and survival in patients with BC. Electronic databases were searched.

Drosophila UTX coordinates with p53 to regulate ku80 expression in response to DNA damage.

UTX is known as a general factor that activates gene transcription during development. Here, we demonstrate an additional essential role of UTX in the DNA damage response, in which it upregulates the expression of ku80 in Drosophila, both in cultured cells and in third instar larvae. We further showed that UTX mediates the expression of ku80 by the demethylation of H3K27me3 at the ku80 promoter upon exposure to ionizing radiation (IR) in a p53-dependent manner.