PLOD2 promotes colorectal cancer progression by stabilizing USP15 to activate the AKT/mTOR signaling pathway

Lan, Jiong-Cai; Zhang, Sijing; Zheng, Lin; Long, Xiaoli; Chen, Jianxiong; Liu, Xunhua; Zhou, Miao; Zhou, Jun

doi:10.1111/cas.15851

Cited by 8 publications

(2 citation statements)

References 33 publications

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“…Both in vivo and in vitro studies have demonstrated that PLOD2 knockdown inhibits the proliferation, invasion, and anchorage-independent growth of GBM ( 108 , 110 , 111 ). Minoxidil, a confirmed PLOD2 inhibitor ( 112 ), could suppress tumor metastasis, in part, by reversing collagen cross-linking in ECM ( 113 , 114 ). Moreover, studies have found that minoxidil cloud increases the antitumor drug permeability of the blood-brain tumor barrier, resulting in improved and selective delivery to brain tumors, including GBM ( 115 , 116 ).…”

Section: Antifibrosis Therapies Explored and Tested In Gliomamentioning

confidence: 99%

The tumor-associated fibrotic reactions in microenvironment aggravate glioma chemoresistance

Xu,

Zhang,

Chen

et al. 2024

Front. Oncol.

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Malignant gliomas are one of the most common and lethal brain tumors with poor prognosis. Most patients with glioblastoma (GBM) die within 2 years of diagnosis, even after receiving standard treatments including surgery combined with concomitant radiotherapy and chemotherapy. Temozolomide (TMZ) is the first-line chemotherapeutic agent for gliomas, but the frequent acquisition of chemoresistance generally leads to its treatment failure. Thus, it’s urgent to investigate the strategies for overcoming glioma chemoresistance. Currently, many studies have elucidated that cancer chemoresistance is not only associated with the high expression of drug-resistance genes in glioma cells but also can be induced by the alterations of the tumor microenvironment (TME). Numerous studies have explored the use of antifibrosis drugs to sensitize chemotherapy in solid tumors, and surprisingly, these preclinical and clinical attempts have exhibited promising efficacy in treating certain types of cancer. However, it remains unclear how tumor-associated fibrotic alterations in the glioma microenvironment (GME) mediate chemoresistance. Furthermore, the possible mechanisms behind this phenomenon are yet to be determined. In this review, we have summarized the molecular mechanisms by which tumor-associated fibrotic reactions drive glioma transformation from a chemosensitive to a chemoresistant state. Additionally, we have outlined antitumor drugs with antifibrosis functions, suggesting that antifibrosis strategies may be effective in overcoming glioma chemoresistance through TME normalization.

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Section: Antifibrosis Therapies Explored and Tested In Gliomamentioning

confidence: 99%

The tumor-associated fibrotic reactions in microenvironment aggravate glioma chemoresistance

Xu,

Zhang,

Chen

et al. 2024

Front. Oncol.

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“…Further, the acetylation level of eEF1A1 K439 was higher in CRC patients than in healthy individuals [119]. Procollagen-lysine, 2-oxoglutarate 5-dioxygenase 2 (PLOD2) serves as a lysyl hydroxylase, which has been found to interact with USP15, which promotes CRC invasion and metastasis via activating the AKT/mTOR pathway [120] (Figure 6).…”

Section: Non-classical Ptms and Crc Metastasismentioning

confidence: 99%

Role of Post-Translational Modifications in Colorectal Cancer Metastasis

Peng,

Liu,

Hai

et al. 2024

Cancers

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Colorectal cancer (CRC) is one of the most common malignant tumors of the digestive tract. CRC metastasis is a multi-step process with various factors involved, including genetic and epigenetic regulations, which turn out to be a serious threat to CRC patients. Post-translational modifications (PTMs) of proteins involve the addition of chemical groups, sugars, or proteins to specific residues, which fine-tunes a protein’s stability, localization, or interactions to orchestrate complicated biological processes. An increasing number of recent studies suggest that dysregulation of PTMs, such as phosphorylation, ubiquitination, and glycosylation, play pivotal roles in the CRC metastasis cascade. Here, we summarized recent advances in the role of post-translational modifications in diverse aspects of CRC metastasis and its detailed molecular mechanisms. Moreover, advances in drugs targeting PTMs and their cooperation with other anti-cancer drugs, which might provide novel targets for CRC treatment and improve therapeutic efficacy, were also discussed.

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USP15 as a Potential Therapeutic Target in Cerebral Ischemia: Modulation of Ferroptosis and Cognitive Dysfunction via the Nrf2/GPX4 Axis in Mice

Yi,

Xiao,

Lei

et al. 2024

Neuromol Med

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PLOD2 promotes colorectal cancer progression by stabilizing USP15 to activate the AKT/mTOR signaling pathway

Cited by 8 publications

References 33 publications

The tumor-associated fibrotic reactions in microenvironment aggravate glioma chemoresistance

The tumor-associated fibrotic reactions in microenvironment aggravate glioma chemoresistance

Role of Post-Translational Modifications in Colorectal Cancer Metastasis

USP15 as a Potential Therapeutic Target in Cerebral Ischemia: Modulation of Ferroptosis and Cognitive Dysfunction via the Nrf2/GPX4 Axis in Mice

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