SIK1 (Salt Inducible Kinase 1)

Both the authors and the Editor of International Journal of Molecular Medicine apologize to the readership for any inconvenience caused. [International Journal of Molecular Medicine 37: 1601‑1610, 2016; DOI: 10.3892/ijmm.2016.2553].

Isoform selectivity of 27 was confirmed in a cellular context. Identification of compound 27 provided a SIK1-selective compound to investigate the role of SIK1 in biological processes mediated by SIKs; however, activity of 27 on other kinases, in particular tyrosine kinases, should not be neglected upon data interpretation.

Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [International Journal of Molecular Medicine 37: 1601‑1610, 2016; DOI: 10.3892/ijmm.2016.2553].

Our findings suggest that miR-17-5p may promote lung adenocarcinoma by targeting SIK1 and may be a potential biomarker for lung cancer.

Targeting SIK1 could significantly reverse ferroptosis resistance and enhance cytotoxic effects of gemcitabine via increasing ferroptosis sensitivity in PDAC cells...These findings unveil a crucial mechanism through which PDAC counters ferroptosis via SIK1-mediated HDAC5 stabilization and subsequent SLC7A11 upregulation. This study underscores the promising potential of targeting SIK1-HDAC5 axis as a therapeutic strategy to overcome drug resistance in PDAC.

Conversely, subtype C2 patients showed higher expression of NTRK2, STAT3, SIK1, AKT1, and EGFR, suggesting these genes as promising therapeutic targets for C2 subtype liver cancer. Furthermore, employing Weighted Correlation Network analysis, machine learning models, and experimental validation, we identified NPY1R and HGF as potential biomarkers for the diagnosis and treatment of liver cancer.

PDO-based NAC shows a promising resectable rate in BRPC patients, with good tolerance. Potential drug-resistant and sensitive genes and cell-cell interaction changes may participate in the development of gemcitabine resistance.

Moreover, stimulated HUVECs could secrete the chemokine CCL20 and induce HCC progression and metastasis through the CCL20/CCR6 signal pathway in vitro and in vivo. The findings indicated that miR-183-5p delivered by EVs from HCC cells is crucial in mediating the communication between HUVECs and HCC cells by modulating the SIK1/PI3K/AKT and CCL20/CCR6 signaling pathways, and EVs-miR-183-5p might be a potential therapeutic target for HCC patients.

It has been suggested that danger signals from RhE, in response to DNCB, enhance the expression of these genes in THP-1 cells. We clarified the effects of the medium and co-culture and proposed these five genes as potential markers for skin sensitization evaluation.

The role of SIKs in cancer progression and metastasis involves complex mechanisms that vary among cancer types. Additionally, research on SIK inhibitors suggests that targeting these kinases might offer promising avenues for improving cancer treatment outcomes.

Moreover, YKL-06-061 effectively enhanced the antiproliferation of gemcitabine or doxorubicin in pancreatic cancer cells in a synergistic manner. Collectively, these findings implicate YKL-06-061 as a promising therapeutic agent for patients with pancreatic cancer.

Differentially expressed systemic mRNAs that are linked to mitochondrial function, oxidative stress, and inflammation may have a role in the pathology of wAMD. Our observations provide new data for the understanding of the progression of wAMD.