The roles and mechanisms of SREBP1 in cancer development and drug response.

Cancer occurrence and development are closely related to increased lipid production and glucose consumption. Lipids are the basic component of the cell membrane and play a significant role in cancer cell processes such as cell-to-cell recognition, signal transduction, and energy supply, which are vital for cancer cell rapid proliferation, invasion, and metastasis. Sterol regulatory element-binding transcription factor 1 (SREBP1) is a key transcription factor regulating the expression of genes related to cholesterol biosynthesis, lipid homeostasis, and fatty acid synthesis.

E3 ubiquitin ligase RNF148 functions as an oncogene in colorectal cancer by ubiquitination-mediated degradation of CHAC2.

We previously reported that RNF148 was involved in the ubiquitination-mediated degradation of CHAC2. However, its molecular mechanism was not determined. In this study, we investigated the role and mechanism of RNF148 in the progression of colorectal cancer (CRC), especially in the process of ubiquitination-mediated degradation of CHAC2.

The Biological Functions and Regulatory Mechanisms of Fatty Acid Binding Protein 5 in Various Diseases.

In recent years, fatty acid binding protein 5 (FABP5), also known as fatty acid transporter, has been widely researched with the help of modern genetic technology. Emerging evidence suggests its critical role in regulating lipid transport, homeostasis, and metabolism. Its involvement in the pathogenesis of various diseases such as metabolic syndrome, skin diseases, cancer, and neurological diseases is the key to understanding the true nature of the protein.

The mechanism of mA methyltransferase METTL3-mediated autophagy in reversing gefitinib resistance in NSCLC cells by β-elemene.

N-methyladenosine (mA) modification can alter gene expression by regulating RNA splicing, stability, translocation, and translation. Emerging evidence shows that mA modification plays an important role in cancer development and progression, including cell proliferation, migration and invasion, cell apoptosis, autophagy, and drug resistance. Until now, the role of mA modification mediated autophagy in cancer drug resistance is still unclear.

METTL3 plays multiple functions in biological processes.

N-methyladenosine (mA) is the most common internal modification of mRNAs in higher eukaryotic. This process is performed by methyltransferase. Methyltransferase-like 3 (METTL3) is the best known mA methyltransferase that functions in the reversible epi-transcriptome modulation of mA modification.

β-Elemene Reverses the Resistance of p53-Deficient Colorectal Cancer Cells to 5-Fluorouracil by Inducing Pro-death Autophagy and Cyclin D3-Dependent Cycle Arrest.

Objective: Colorectal cancer is a malignant tumor of the digestive system with high morbidity and mortality. 5-fluorouracil remains a widely used chemotherapeutic drug in the treatment of advanced colorectal cancer, but chemotherapy drugs are prone to develop drug resistance, p53 deletion or mutation is an important reason for the resistance of colorectal cancer cells to 5-fluorouracil. β-elemene has been proved to have the potential of reverse chemotherapy drug resistance, but the mechanism is unknown.

Erianin, a novel dibenzyl compound in Dendrobium extract, inhibits lung cancer cell growth and migration via calcium/calmodulin-dependent ferroptosis.

Ferroptosis, a novel form of programmed cell death, is characterized by iron-dependent lipid peroxidation and has been shown to be involved in multiple diseases, including cancer. Stimulating ferroptosis in cancer cells may be a potential strategy for cancer therapy. Therefore, ferroptosis-inducing drugs are attracting more attention for cancer treatment.

The roles and mechanisms of YTH domain-containing proteins in cancer development and progression.

Evolutionarily conserved YT521-B homology (YTH) domain-containing proteins, including YTHDF1-3 and YTHDC1-2, are known to confer mA-dependent RNA-binding activity. The YTH domain-containing proteins participate in numerous RNA processes, such as mRNA splicing, nuclear export, translation and decay in post-transcriptional regulation. Most recently, it has been found that YTH domain-containing proteins play important roles in post-transcriptional modification process hence modulate the expression of genes involved in cancer and other processes including cell cycle progression, cell proliferation, migration and invasion, inflammatory, immunity and autophagy.

Combinative treatment of β-elemene and cetuximab is sensitive to KRAS mutant colorectal cancer cells by inducing ferroptosis and inhibiting epithelial-mesenchymal transformation.

: RAS mutations limit the effectiveness of anti-epidermal growth factor receptor (EGFR) monoclonal antibodies in combination with chemotherapy for metastatic colorectal cancer (mCRC) patients. Therefore, new cell death forms have focused on identifying indirect targets to inhibit Ras-induced oncogenesis. Recently, emerging evidence has shown the potential of triggering ferroptosis for cancer therapy, particularly for eradicating aggressive malignancies that are resistant to traditional therapies.

The emerging molecular mechanism of mA modulators in tumorigenesis and cancer progression.

N-methyladenosine (mA) is the most abundant RNA modification; mA modifications are installed by methyltransferases, removed by demethylases and recognized by reader proteins. MA plays crucial roles in a variety of biological processes by regulating target RNA translation, splicing, nuclear export, and decay. Since the establishment of methylated RNA immunoprecipitation-sequencing methodology, over three hundred articles about mA modulators, including "writers", "erasers" and "readers", have been reported in the last four years.

PCDH17 increases the sensitivity of colorectal cancer to 5-fluorouracil treatment by inducing apoptosis and autophagic cell death.

5-Fluorouracil (5-FU) is known as a first-line chemotherapeutic agent against colorectal cancer (CRC), but drug resistance occurs frequently and significantly limits its clinical success. Our previous study showed that the protocadherin 17 () gene was frequently methylated and functioned as a tumor suppressor in CRC. However, the relationship between and 5-FU resistance in CRC remains unclear.