Erratum to: "Fer exacerbates renal fibrosis and can be targeted by miR-29c-3p".

[This corrects the article DOI: 10.1515/med-2021-0319.].

Fer exacerbates renal fibrosis and can be targeted by miR-29c-3p.

Aim: Renal fibrosis (RF) is a common clinical condition leading to irreversible renal function loss. Tyrosine kinase proteins and microRNAs (miRs) are associated with pathogenesis and we aim to investigate the role of Fer and its partner miR(s) in RF.

Method: reproduction of Mouse Kidney FibrOmics browser was performed to identify potential miR(s) and target gene(s).

microRNA let-7i-5p aggravates kidney fibrosis via targeting GALNT1.

Renal fibrosis poses critical health problem. We aimed to investigate role of let-7i-5p in renal fibrosis. In silico reproduction of Mouse Kidney FibrOmics browser was used to identify potential target of let-7i-5p.

circPRRC2A promotes angiogenesis and metastasis through epithelial-mesenchymal transition and upregulates TRPM3 in renal cell carcinoma.

: Circular RNAs (circRNAs) have been identified as essential regulators in a plethora of cancers. Nonetheless, the mechanistic functions of circRNAs in Renal Cell Carcinoma (RCC) remain largely unknown. : In this study, we aimed to identify novel circRNAs that regulate RCC epithelial-mesenchymal transition (EMT), and to subsequently determine their regulatory mechanisms and clinical significance.

Overexpression of CKAP4 is Associated with Poor Prognosis in Clear Cell Renal Cell Carcinoma and Functions via Cyclin B Signaling.

We aimed to study the role of CKAP4 in clear cell renal cell carcinoma (ccRCC), which is not reported previously. In silico exploration and validation using immunohistochemistry in ccRCC samples were used to identify the impact of CKAP4 expression on clinicopathological parameters. In vitro and in vivo studies were carried out to recapitulate the role of CKAP4 in ccRCC cell lines and animal models.

Genetic alteration in phosphofructokinase family promotes growth of muscle-invasive bladder cancer.

Aims: Metabolic alterations in cancer, including bladder cancer, have been addressed in recent years. We aimed to study the role of phosphofructokinase (PFK) in muscle-invasive bladder cancer (MIBC).

Method: By in silico analysis of the bladder cancer data from the Cancer Genome Atlas (TCGA) database using the cBioPortal platform, we studied genetic alteration of genes within the PFK family (PFKL, PFKM, PFKP, PFKFB1, PFKFB2, PFKFB3, and PFKFB4).