Cancer Science

Our results demonstrated that circARHGEF28 suppressed prostate cancer (PCa) progression through inactivating the nuclear factor kappa-B (NF-κB) pathway via the miR-671-5p/LGALS3BP axis, indicating that the circARHGEF28/miR-671-5p/LGALS3BP/NF-κB axis is a promising therapeutic target in PCa.

(1) PPARγ acts as an autophagic receptor for PD-L1 autophagic degradation. (2) Agonist enhanced PD-1 antibody against NSCLC tumor immune escape. (3) PPARγ agonist could be a therapic strategy for antitumor immunotherapy of NSCLC. (1) PPARγ induced PD-L1 autophagic degradation. (2) Loss of PPARγ led to NSCLC tumor immune escape. (3) PPARγ acts as autophagic receptor for PD-L1 autophagic degradation

FK506 binding protein FKBP52 is associated with hormone-dependent, stress-related, and neurodegenerative diseases, revealing its diverse functions. In particular, FKBP52 promotes the growth of hormone-dependent cancers by activating steroid hormone receptors.

Pemetrexed might enhance the expression and glycosylation of HLA-G and PD-L1, which could provide a beneficial TME for CTL cytotoxicity against NSCLC. Dual targeting of PD-L1 and HLA-G combined with pemetrexed might have a better extent of CTL-based immunotherapy.

Neoadjuvant chemoimmunotherapy for non–small-cell lung cancer (NSCLC) has achieved an excellent pathological response. The dynamic changes in the tumor immune microenvironment are closely related to the efficacy of neoadjuvant immunotherapy in NSCLC patients. Some special gene alterations, such as ATR kinase, are associated with immune infiltrations and better pathological response using neoadjuvant immunotherapy treatment.

The stimulation of BW5147.3 cells expressing objective TCRs with a single dose of antigenic peptides and analysis combining the expression of CD69, CD137, and PD1 allows us to select highly responsive T cell receptors.

We provided a novel concept that CD69 is strongly expressed in epithelial, nonhematological ovarian clear cell carcinoma (CCC) cells. CD69 protein induced in response to fatty acid and oxygen starvation is responsible for fibronectin-driven epithelial–mesenchymal transition, potentially contributing to the poor prognosis of CCC patients.

AGR2 in malignant cells regulates cell-cell communication by coordinating cytokine-chemokine signaling and immune infiltration. AGR2 could affect tumor immune microenvironment and thus promoted the progression of breast cancer.

TRIM36 can promote the occurrence of ferroptosis and finally inhibit the NED of PCa (prostate cancer) cells by inhibiting the ferroptosis-related gene glutathione peroxidase 4 through hexokinase 2 in the ubiquitin glycolysis pathway. This mechanism has great potential to design new strategies to retard NEPC and may help prostate cancer researchers to find potential therapeutic targets for treating NEPC.

In the present study, we evaluated the potential mechanism(s) of STAT3-induced 5-fluorouracil (5-Fu) resistance in colorectal cancer (CRC). Our results show that STAT3 regulates 5-Fu resistance in CRC by promoting Mcl-1–dependent cytoprotective autophagy. Our results provide a novel role of STAT3 and may offer a new approach for the management of CRC 5-Fu resistance.

Tumor-associated macrophages (TAMs) are the most prominent immune cells in the breast cancer microenvironment, and the protumor functions of TAMs are thought to affect cancer progression and resistance to anti-cancer therapy. Recent advances have highlighted the significant involvement of TAMs in the resistance of breast cancer cells to immunotherapy.

Harboring a high expression level of m6A reader HNRNPC, progressed prostate cancer (PCa) exhibited a “cold” immune phenotype, which was mainly induced by increasing Treg abundance. Targeting HNRNPC may help activate the immune microenvironment or elevate the sensitiveness to anti-CTLA4 therapies.

In this study, we revealed that IFN-γ-STAT1-mediated NK2R expression is involved in the induction of antitumor effector CD8+ T cells in the tumor microenvironment, which contributes to suppressing the tumorigenesis of liver cancer cells in vivo.

We generated an immunocompetent mouse model to study our oncolytic virus, designated as rMV-SLAMblind. We evaluated the induction of immune responses after rMV-SLAMblind cancer therapy with this model.

Clinical proteomics has become increasingly important in recent years. In this review, we provide an overview of state-of-the-art mass spectrometry techniques in cancer research and describe our targeted glycoform analysis for the development of specific cancer biomarkers and our immunopeptidomics studies for the identification of tumor-specific immunopeptides.

Here, we focused on cell line morphology in 3D cultures and xenograft tumors. In the bronchial epithelial phenotype, most of the cell lines displayed a round morphology in 3D culture, and some of them showed acinar or papillary patterns and desmoplastic reactions in xenograft tumors. In contrast, the non-bronchial epithelial phenotype cell lines frequently displayed stellate or grape-like morphologies in 3D culture and showed solid patterns with no desmoplastic reactions in xenograft tumors. This study serves as an excellent resource for lung adenocarcinoma cell lines with clinically relevant information on molecular and morphological characteristics.

We review the epigenetic dysregulation arising in cancer cells that disseminates throughout the TME, which resulted in the inhibition of antitumor immunity.

We investigated the effects of gemcitabine plus cisplatin (GC) chemotherapy on the gut microbiome and determined whether oral supplementation with a probiotics mixture of Lactobacillus casei Shirota and Bifidobacterium breve could improve the anti-tumor response induced by GC chemotherapy. We found altered levels of gut microbiota and increased infiltration of CD8⁺ T cells and dendritic cells in the tumor microenvironment of GC + probiotics group compared with the GC group. We believe that our study makes a significant contribution to the literature, because our findings highlight the anti-tumor responses induced by a probiotics mixture of Lactobacillus and Bifidobacterium during GC chemotherapy.

By combining the organoid culture and xenograft formation, a novel cell line HS-1 was eventually established from a biopsy of acinar cell carcinoma (ACC), a rare subtype of pancreatic cancer, for the first time as an organoid. HS-1 is positive for carboxylic ester hydrolase (CEH), a highly specific acinar cell marker, and secretes trypsin abundantly, but is negative for the duct cell marker CD133, thereby retaining the features of acinar cells and the original tumor. HS-1 harbors a missense mutation in EP400 and a 30-Mb deletion encompassing CDKN2A. Drug screening identified the proteasome inhibitor bortezomib as a potential ACC therapeutic. This cell line will be useful for further ACC studies.

The authors found that coxsackievirus A11 (CVA11) infection exhibited a marked oncolytic activity in multiple human malignant pleural mesothelioma cell lines in vitro, and that serial intratumoral CVA11 injections into mesothelioma xenografts resulted in significant suppression of tumor growth in SCID mice with tolerability. The authors successfully identified ICAM-1 as a receptor for CVA11 infection. CVA11 infection-triggered cytotoxicity was partially dependent on MEK/ERK and PI3K/Akt signaling pathways and manifested multimodal immunogenic cell death with proinflammatory cytokine and DAMPs.