LAPTM5 regulated by FOXP3 promotes the malignant phenotypes of breast cancer through activating the Wnt/β‑catenin pathway

Han, Sijia; Jin, Xueying; Hu, Tianyu; Chi, Feng

doi:10.3892/or.2023.8497

Cited by 4 publications

(3 citation statements)

References 54 publications

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“…Accumulating evidence has revealed that the dysregulation of the Wnt/ β -catenin signal pathway contributes to the development and progression of several solid tumors and hematological malignancies ( Di Bartolomeo et al, 2023 ; Han et al, 2023 ; Li et al, 2022 ; Muto et al, 2023 ). In this study, we discovered that the Wnt/ β -catenin signal pathway was also abnormally expressed in ccRCC, suggesting the involvement of Wnt/ β -catenin in ccRCC.…”

Section: Discussionmentioning

confidence: 99%

TTC13 expression and STAT3 activation may form a positive feedback loop to promote ccRCC progression

Xie,

Fang,

Chen

et al. 2023

PeerJ

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Background Renal cell carcinoma (RCC) originates from renal tubular epithelial cells and is mainly classified into three histological types, including clear cell renal cell carcinoma (ccRCC) which accounts for about 75% of all kidney cancers and is characterized by its strong invasiveness and poor prognosis. Hence, it is imperative to understand the mechanisms underlying the occurrence and progression of ccRCC to identify effective biomarkers for the early diagnosis and the prognosis prediction. Methods The mRNA level of TTC13 was quantified by RT-PCR, while the protein level was determined by western blot and immunohistochemistry (IHC) staining. Cell proliferation was measured by cck-8, and cell apoptosis was detected by flow cytometry. The binding of STAT3 to the promoter region of TTC13 was determined by the luciferase reporter assay and chip experiments. STAT3 nuclear translocation was assessed by immunofluorescence staining. Results We found that TTC13 was up-regulated in ccRCC, and TTC13 promoted cell proliferation as well as inhibited cell apoptosis and autophagy of ccRCC through wnt/β-catenin and IL6-JAK-STAT3 signaling pathways. Furthermore, TTC13 might play a role in the immune infiltration and immunotherapy of ccRCC. Mechanistically, STAT3 activated the transcription of TTC13 gene. Conclusions STAT3 directly regulated TTC13 expression through a positive feedback loop mechanism to promote ccRCC cell proliferation as well as reduce cell apoptosis and autophagy. These findings suggested new and effective therapeutic targets for more accurate and personalized treatment strategies.

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Section: Discussionmentioning

confidence: 99%

TTC13 expression and STAT3 activation may form a positive feedback loop to promote ccRCC progression

Xie,

Fang,

Chen

et al. 2023

PeerJ

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“…Increased expressions of lysosomal membrane proteins and cysteine cathepsins are associated with the upregulation of EMT marker proteins, induction of mesenchymal phenotype, and treatment resistance [ 281 , 282 , 283 , 284 , 285 ]. Induction of EMT is often regulated by TGF-β signaling, and inhibition of cysteine cathepsins can reverse this process and attenuate invasive growth [ 284 , 286 , 287 ].…”

Section: Lysosomal Involvement In Cancermentioning

confidence: 99%

Lysosomes in Cancer—At the Crossroad of Good and Evil

Eriksson,

Öllinger

2024

Cells

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Although it has been known for decades that lysosomes are central for degradation and recycling in the cell, their pivotal role as nutrient sensing signaling hubs has recently become of central interest. Since lysosomes are highly dynamic and in constant change regarding content and intracellular position, fusion/fission events allow communication between organelles in the cell, as well as cell-to-cell communication via exocytosis of lysosomal content and release of extracellular vesicles. Lysosomes also mediate different forms of regulated cell death by permeabilization of the lysosomal membrane and release of their content to the cytosol. In cancer cells, lysosomal biogenesis and autophagy are increased to support the increased metabolism and allow growth even under nutrient- and oxygen-poor conditions. Tumor cells also induce exocytosis of lysosomal content to the extracellular space to promote invasion and metastasis. However, due to the enhanced lysosomal function, cancer cells are often more susceptible to lysosomal membrane permeabilization, providing an alternative strategy to induce cell death. This review summarizes the current knowledge of cancer-associated alterations in lysosomal structure and function and illustrates how lysosomal exocytosis and release of extracellular vesicles affect disease progression. We focus on functional differences depending on lysosomal localization and the regulation of intracellular transport, and lastly provide insight how new therapeutic strategies can exploit the power of the lysosome and improve cancer treatment.

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“…LAPTM5 is a transmembrane receptor that localizes to intracellular vesicles and endosomes/lysosomes and transports proteins to lysosomes for degradation 9,10 . LAPTM5 acts as an oncogene and promotes malignant phenotypes, including metastatic potential, proliferation, and resistance to treatment 11,12 .…”

Section: Introductionmentioning

confidence: 99%

HIF-1α/LAPTM5/STAT1 axis promotes the malignant progression of clear cell renal cell carcinoma

Li,

Zhang,

Zhang

et al. 2023

Preprint

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Clear cell renal cell carcinoma (ccRCC) is the most common type of kidney cell carcinoma with poor prognosis and high mortality. Mutation-mediated inactivation of Von Hippel Lindau (VHL) is a hallmark feature of ccRCC, and it leads to the accumulation of hypoxia-inducible factors (HIFs) and cancer progression. Therefore, further elucidation of the network that regulates the VHL/HIF-1α pathway will provide potential therapeutic targets for the treatment of ccRCC. The results of the current study demonstrated that lysosomal-associated protein transmembrane 5 (LAPTM5) is a novel transcriptional target of HIF-1α and that HIF-1α positively regulates the expression of LAPTM5 in ccRCC cells. Furthermore, the maximum overexpression of LAPTM5 in ccRCC tissues compared with corresponding normal tissues was observed in the pan-cancer analysis. In addition, LAPTM5 overexpression was closely related to metastasis and poor outcomes in ccRCC patients. In addition, LAPTM5 promoted the proliferation, migration and invasion of ccRCC cells. Mechanistically, LAPTM5 regulated the K63-linked ubiquitination of STAT1, enhanced the interaction between STAT1 and JAK2, and induced the phosphorylation of STAT1 at Y701, ultimately promoting the progression of ccRCC. This study reveals a novel HIF-1α/LAPTM5/STAT1 signalling pathway that promotes ccRCC progression and provides potential therapeutic strategies for the treatment of ccRCC.

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LAPTM5 regulated by FOXP3 promotes the malignant phenotypes of breast cancer through activating the Wnt/β‑catenin pathway

Cited by 4 publications

References 54 publications

TTC13 expression and STAT3 activation may form a positive feedback loop to promote ccRCC progression

TTC13 expression and STAT3 activation may form a positive feedback loop to promote ccRCC progression

Lysosomes in Cancer—At the Crossroad of Good and Evil

HIF-1α/LAPTM5/STAT1 axis promotes the malignant progression of clear cell renal cell carcinoma

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