CD14, a novel surface marker of esophageal cancer stem cells

Yong-gang, Lin; Dong, Jianjiang; Yu, Wei; Li, Yufei; Liu, Zhixin; Liu, Jiaqi; Wang, Cuiju; Qin, Jian; Zhu, Liting; Liang, Jun

doi:10.3892/or.2022.8450

Cited by 3 publications

(3 citation statements)

References 62 publications

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“…suggesting also that CD14 may be linked to CCSCs (16)(17)(18). Furthermore, a previous study by the authors revealed that esophageal CSCs expressed CD14, a novel surface marker (19).…”

Section: Regulation Of the Migration Of Colorectal Cancer Stem Cells ...mentioning

confidence: 82%

“…Additionally, CD14 has been linked to tumor recurrence, growth, metastasis and therapy resistance, which is consistent with CSC traits (such as recurrence, growth, metastasis and resistance to therapy), suggesting also that CD14 may be linked to CCSCs ( 16 – 18 ). Furthermore, a previous study by the authors revealed that esophageal CSCs expressed CD14, a novel surface marker ( 19 ).…”

Section: Introductionmentioning

confidence: 95%

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Regulation of the migration of colorectal cancer stem cells via the TLR4/MyD88 signaling pathway by the novel surface marker CD14 following LPS stimulation

Li,

Shi,

Liu

et al. 2023

Oncol Lett

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Cell surface markers are most widely used in the study of cancer stem cells (CSCs). However, cell surface markers that are safely and stably expressed in CSCs have yet to be identified. Colonic CSCs express leukocyte CD14. CD14 binding to the ligand lipopolysaccharide (LPS) is involved in the inflammatory response via the Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88) signaling pathway. TLR4 and MyD88 have been reported to promote the proliferation, metastasis and tumorigenicity of colon cancer cells, which is consistent with the characteristics of CSCs. In the present study, the proposed experimental method to detect cell proliferation, metastasis and tumorigenesis was used to confirm that, under LPS stimulation, CD14 promoted the proliferation, migration and tumorigenesis of colonic CSCs via the TLR4/MyD88 signaling pathway. Cell Counting Kit-8 and 5-ethynyl-2′-deoxyuridine assays were used to assess the proliferation and migration of the cells. Colony formation and nude mouse xenograft assays were used to assess the capacity of cells to form tumors. Using western blotting and reverse transcription-quantitative PCR, the mRNA and protein levels of CD14, TLR4 and MyD88 were examined. It was confirmed that CD14 promoted the proliferation, metastasis and tumorigenesis of colon CSCs in response to LPS stimulation via the TLR4/MyD88 signaling pathway, and CD14 + colon cancer cells were successfully isolated and sorted. According to the results of proliferation assay, it was determined that CD14 regulated the LPS-induced proliferation of colon CSCs. CD14, TLR4 and MyD88 protein and mRNA expression was upregulated in colon CSCs in response to LPS stimulation. This indicates a potential novel target for colon CSC-related studies.

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“…suggesting also that CD14 may be linked to CCSCs (16)(17)(18). Furthermore, a previous study by the authors revealed that esophageal CSCs expressed CD14, a novel surface marker (19).…”

Section: Regulation Of the Migration Of Colorectal Cancer Stem Cells ...mentioning

confidence: 82%

Section: Introductionmentioning

confidence: 95%

Regulation of the migration of colorectal cancer stem cells via the TLR4/MyD88 signaling pathway by the novel surface marker CD14 following LPS stimulation

Li,

Shi,

Liu

et al. 2023

Oncol Lett

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“…The TWIST1-JAGGED1-NOTCH-KLF4 axis induces stem cell-like features and metastasis, where KLF4 and BMI1 contribute to TWIST1-induced tumor-initiating capacity, and knockdown of BMI1 expression leads to a reduction in the size and number of tumor spheroids [14]. Cluster of differentiation (CD), a class of proteins present on the cell membrane, such as CD14 [15], CD44 [16], and CD47/ CD133 [17], can also serve as a surface marker of ESCC stem cells and inhibit the maintenance of tumor stemness by suppressing its expression, making it an independent prognostic factor and a promising therapeutic target for ESCC stem cells.…”

Section: Cancer Stem Cellsmentioning

confidence: 99%

Mechanisms of radiotherapy resistance and radiosensitization strategies for esophageal squamous cell carcinoma

An,

Li,

Jia

2023

Mol Cancer

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Esophageal squamous cell carcinoma (ESCC) is the sixth most common cause of cancer-related mortality worldwide, with more than half of them occurred in China. Radiotherapy (RT) has been widely used for treating ESCC. However, radiation-induced DNA damage response (DDR) can promote the release of cytokines and chemokines, and triggers inflammatory reactions and changes in the tumor microenvironment (TME), thereby inhibiting the immune function and causing the invasion and metastasis of ESCC. Radioresistance is the major cause of disease progression and mortality in cancer, and it is associated with heterogeneity. Therefore, a better understanding of the radioresistance mechanisms may generate more reversal strategies to improve the cure rates and survival periods of ESCC patients. We mainly summarized the possible mechanisms of radioresistance in order to reveal new targets for ESCC therapy. Then we summarized and compared the current strategies to reverse radioresistance.

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Cancer Immunotherapies Targeting Cancer Stem Cells: Concepts, Applications, and Advances

Farhangnia,

Shokri,

Akbarpour

et al. 2024

Interdisciplinary Cancer Research

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CD14, a novel surface marker of esophageal cancer stem cells

Cited by 3 publications

References 62 publications

Regulation of the migration of colorectal cancer stem cells via the TLR4/MyD88 signaling pathway by the novel surface marker CD14 following LPS stimulation

Regulation of the migration of colorectal cancer stem cells via the TLR4/MyD88 signaling pathway by the novel surface marker CD14 following LPS stimulation

Mechanisms of radiotherapy resistance and radiosensitization strategies for esophageal squamous cell carcinoma

Cancer Immunotherapies Targeting Cancer Stem Cells: Concepts, Applications, and Advances

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