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The authors identified a novel long non-coding RNA (lncRNA), DLGAP1-AS1, that exhibits oncogenic. properties in non-small-cell lung cancer (NSCLC). DLGAP1-AS1 was highly expressed in NSCLC. tissues and cells. Inhibition of lncRNA DLGAP1-AS1 suppressed NSCLC progression both in vitro and. in vivo via the miR-193a-5p/denticleless protein homolog (DTL) axis. This novel regulatory network. provides a potential therapeutic strategy for NSCLC.

Ubiquitin-specific protease 3 (USP3), a cysteine protease, is deubiquitinating enzyme. USP3 is aberrantly expressed in several types of tumors. The authors show that USP3 is an important positive regulator in gallbladder cancer progression, and that pyruvate kinase L/R plays a key role in the progression of GBC.

The authors present a workflow that allows the simultaneous measurement of the whole exome and the transcriptome by next-generation sequencing from formalin-fixed paraffin-embedded tissue sections that were analyzed by matrix-assisted laser desorption ionization mass spectrometry imaging. The data and analyses demonstrate the feasibility and reproducibility of this approach, which expands the possibilities of multi-omics integration in cancer research.

For precancerous/endometrial cancer patients with fertility maintain desire, progestin resistance is the main obstacle of conservative therapy. The authors found that brusatol, as a natural compound, suppresses progestin metabolism through regulating the NRF2-TET1-AKR1C1 pathway to sensitize precancerous/endometrial cancers to progestin and relieve progestin resistance. This study indicates that progestin combined with brusatol may enhance the treatment effects and that AKR1C1 expression patterns may serve as an important biomarker of progestin resistance in endometrial cancer.

Non-small cell lung cancer (NSCLC) is the most common type of lung cancer and is associated with limited treatment options. This study elucidates the role of KLHL17 in the development and progression of NSCLC using clinical samples and NSCLC cell lines. The results show that upregulated KLHL17 in NSCLC promotes the proliferation and migration of tumor by activating Ras/MAPK signaling pathway, and suggest that KLHL17 may be a novel therapeutic target for the treatment of NSCLC.

The authors describe a regulatory mechanism for ferroptosis sensitivity that is dependent on circST6GALNAC6 expression levels in bladder cancer. CircST6GALNAC6 inhibits HSPB1 and promotes cell ferroptosis by blocking the phosphorylation site (Ser-15) of HSBP1 and activating the P38 MAPK signaling pathway. Enhancing the expression of circST6GALNAC6 to promote ferroptosis, or using circST6GALNAC6 as a biomarker of ferroptosis sensitivity, is significant for the development and application of ferroptosis intervention methods.

Hyperglycemia induces endoplasmic reticulum stress and increases expression of MAPK10, and 4-phenylbutyric treatment and the knockdown of MAPK10 both alleviate hyperglycaemia-induced myocardial dysfunction, respectively. Therefore, the present study sheds new light on the novel role of MAPK10 in hyperglycemia-induced myocardial dysfunction in db/db mice.

This study shows the potential application of c-Jun phosphorylation upon cisplatin treatment as a biomarker for cisplatin sensitivity in combination with patient-derived tumor organoids (PDOs). We also compared the responses of 6 PDOs to cisplatin with the therapeutic effect of neoadjuvant chemotherapy in 6 matched patients with esophageal squamous cell carcinoma.

Proteomics plays a vital role in biomedical research in the post-genomic era. With the technological revolution and emerging computational tools, proteomic methodology has evolved rapidly in the past decade and shed light on solving complicated biomedical problems. Thus, this mini-review summarizes existing and emerging high-throughput proteomics methodologies, including mass spectrometry, protein pathway array, next-generation tissue microarrays, single-cell proteomics, single-molecule proteomics, Luminex, Simoa and OLINK Proteomics.

GPM6A expression is markedly suppressed in hepatocellular carcinoma and suppresses proliferation and migration of hepatoma cells. Moreover, its low expression is most likely attributed to upregulated miRNA-96-5p but not gene mutation or changes in methylation. These findings indicate that GPM6A may function as an inhibitory gene in chronic information, fibrosis and oncogenic transformation.

This study presents a novel perspective on the influences of the microbiome-cancer axis during tumor development and treatment, in a syngeneic, immunocompetent mammary tumor mouse model. The findings define substantial remodeling of the gut microbiome and changes in the intestinal immune network in response to the orally administered therapeutic Hedgehog inhibitor, Vismodegib, and highlight the dynamic shifts in the abundance of pro- and anti-inflammatory gut microbes during tumor progression and in response to Hedgehog blockade.

The authors identified tissue inhibitor of metalloproteinase-1 (TIMP1) as an important regulator of tissue stiffness in isocitrate dehydrogenase (IDH)-wild type (WT) gliomas. TIMP1 knockdown decreases tissue stiffness, inhibited the expression of tenascin C and fibronectin, and suppressed tumor progression. These results suggest that TIMP1 could be a potential therapeutic target for IDH-WT gliomas.