Non-oxidative pentose phosphate pathway controls regulatory T cell function by integrating metabolism and epigenetics.

Regulatory T (T) cells are critical for maintaining immune homeostasis and preventing autoimmunity. Here, we show that the non-oxidative pentose phosphate pathway (PPP) regulates T function to prevent autoimmunity. Deletion of transketolase (TKT), an indispensable enzyme of non-oxidative PPP, in T cells causes a fatal autoimmune disease in mice, with impaired T suppressive capability despite regular T numbers and normal Foxp3 expression levels.

PPT1 Reduction Contributes to Erianin-Induced Growth Inhibition in Oral Squamous Carcinoma Cells.

The anticancer properties of erianin have been recently discovered. However, the antitumor effect of erianin in oral squamous cell carcinoma (OSCC) remains unclear. In this study, we demonstrated that erianin can hamper OSCC cells growth both and .

Kynurenine derivative 3-HAA is an agonist ligand for transcription factor YY1.

The 3-hydroxyanthranilic acid (3-HAA), a derivative of kynurenine, was reported to suppress tumor growth. However, the function of 3-HAA largely remains unclear. Here, we report that 3-hydroxyanthranilic acid (3-HAA) is lower in tumor cells, while adding exogenous 3-HAA induces apoptosis in hepatocellular carcinoma by binding YY1.

3-hydroxyanthranic acid increases the sensitivity of hepatocellular carcinoma to sorafenib by decreasing tumor cell stemness.

Sorafenib is the FDA-approved first-line target drug for HCC patients. However, sorafenib only confers 3-5 months of survival benefit with <30% of HCC patients. Thus, it is necessary to develop a sensitizer for hepatocellular carcinoma (HCC) to sorafenib.

The kynurenine derivative 3-HAA sensitizes hepatocellular carcinoma to sorafenib by upregulating phosphatases.

: Sorafenib is the only FDA-approved first-line target drug for HCC patients. However, sorafenib merely confers 3-5 months of survival benefit with less than 30% of HCC patients sensitive to sorafenib therapy. Thus, it's necessary to develop a sensitizer for hepatocellular carcinoma (HCC) to sorafenib.

Targeting the IDO-BCL2A1-Cytochrome c Pathway Promotes Apoptosis in Oral Squamous Cell Carcinoma.

Purpose: Indolamine 2,3-dioxygenase (IDO) is the rate limiting enzyme of tryptophan degradation and is a negative prognostic factor in oral squamous cell carcinoma (OSCC) patients, while the underlying molecular mechanism remains unclear. This research aimed to explore the IDO expression and its biological functions in OSCC.

Materials And Methods: IDO expression was analyzed by qPCR, Western blots, and immunohistochemistry (IHC) in OSCC cell lines and tissue specimens.

Cancer-associated fibroblasts enhance tumor F-FDG uptake and contribute to the intratumor heterogeneity of PET-CT.

Elevated glucose uptake is a hallmark of cancer. Fluorodeoxyglucose (FDG) uptake was believed to indicate the aggressiveness of tumors and the standardized uptake value (SUV) is a well-known measurement for FDG uptake in positron emission tomography-computed tomography (PET/CT). However, the SUV is variable due to the heterogeneity of tumors.

Cancer-associated Fibroblasts Promote Irradiated Cancer Cell Recovery Through Autophagy.

Tumor relapse after radiotherapy is a significant challenge to oncologists, even after recent the advances in technologies. Here, we showed that cancer-associated fibroblasts (CAFs), a major component of cancer stromal cells, promoted irradiated cancer cell recovery and tumor relapse after radiotherapy. We provided evidence that CAFs-produced IGF1/2, CXCL12 and β-hydroxybutyrate were capable of inducing autophagy in cancer cells post-radiation and promoting cancer cell recovery from radiation-induced damage in vitro and in vivo in mice.