Correction: Corrigendum: Adenylate kinase hCINAP determines self-renewal of colorectal cancer stem cells by facilitating LDHA phosphorylation

Abstract

The original version of this Article contained an error in the spelling of the author Zemin Zhang, which was incorrectly given as Zeming Zhang. This has now been corrected in both the PDF and HTML versions of the Article.

Interplay Between Glucose Metabolism and Chromatin Modifications in Cancer

“…LDHA is phosphorylated at tyrosine 10 (Y10) by oncogenic receptor tyrosine kinase FGFR1, which facilitates the formation of active LDHA tetramers (Fan et al, 2011). FGFR1catalyzed LDHA phosphorylation can be enhanced by adenylate kinase hCINAP to augment the catalytic activity of LDHA (Ji et al, 2017). LDHA can also be acetylated and recognized by HSC70, which then delivers LDHA to lysosome to be degraded (Zhao et al, 2013).…”

Unique structural features of the adenylate kinase hCINAP/AK6 and its multifaceted functions in carcinogenesis and tumor progression

“…According to these studies, both overexpressed and endogenous hCINAP showed an obvious nuclear localization. In addition, biochemical approaches such as subcellular fractionation have been employed to examine the localization of endogenous hCINAP [14–16]. These subcellular fractionation assays showed that endogenous hCINAP is localized in both the cytosol and the nucleus.…”

“…Ji et al . [14] identified hCINAP as a potent modulator of metabolic reprogramming in colorectal cancer (CRC) stem cell (CRCSC) proliferation, invasion and metastasis. Mechanistically, hCINAP binds to the C‐terminal domain of LDHA, a key glycolysis regulator, and regenerates ATP to promote fibroblast growth factor receptor 1‐catalyzed LDHA phosphorylation in an AK activity‐dependent manner.…”

“…Ji et al . [14] reported that hCINAP is responsible for the energy requirements of invasive CRCSCs and also that it is a potent modulator of CRCSC metabolic reprogramming, as well as a promising drug target against CRC invasion and metastasis. It is worth notinh that hCINAP inhibition resulted in significant cell death in CRC non‐stem cells and CRCSCs but had no significant effect on apoptosis in colon organoids.…”

“…It is worth notinh that hCINAP inhibition resulted in significant cell death in CRC non‐stem cells and CRCSCs but had no significant effect on apoptosis in colon organoids. Therefore, targeting hCINAP expression and activity in CRC would demonstrate low gut toxicity and comprise a promising therapeutic strategy [14]. Xu et al .…”