Stimuli-induced Organ-specific Injury Enhancement of Organotropic Metastasis in a Spatiotemporal Regulation

Gao, Dongwei; Li, Sha

doi:10.1007/s12253-013-9734-x

Cited by 3 publications

(1 citation statement)

References 214 publications

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“…The development of metastatic lesions at sites of tissue injury has long been recognized for several types of cancer [ 1 ]. The observation that melanoma metastases often appear at wound sites within a few months of trauma suggests that the wound healing process might establish a favorable microenvironment for the adhesion, migration, or proliferation of circulating melanoma cells and thereby promote their colonization [ 2 – 4 ].…”

Section: Introductionmentioning

confidence: 99%

Periostin Is a Key Niche Component for Wound Metastasis of Melanoma

et al. 2015

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Tissue injury promotes metastasis of several human cancers, although factors associated with wound healing that attract circulating tumor cells have remained unknown. Here, we examined the primary and metastatic lesions that appeared 1 month after trauma in a patient with acral lentiginous melanoma. The levels of mRNA for periostin (POSTN), type 1 collagen, and fibronectin were significantly increased in the metastatic lesion relative to the primary lesion. The increase of these extracellular matrix proteins at the wound site was reproduced in a mouse model of wound healing, with the upregulation of Postn mRNA persisting the longest. POSTN was expressed in the region surrounding melanoma cell nests in metastatic lesions of both wounded mice and the patient. POSTN attenuated the cell adhesion and promoted the migration of melanoma cells without affecting their proliferation in vitro. In the mouse model, the wound site as well as subcutaneously injected osteoblasts that secrete large amounts of POSTN invited the metastasis of remotely-transplanted melanoma cells on the sites. Osteoblasts with suppression of POSTN by shRNA showed a greatly reduced ability to promote such metastasis. Our results suggest that POSTN is a key factor in promoting melanoma cell metastasis to wound sites by providing a premetastatic niche.

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Section: Introductionmentioning

confidence: 99%

Periostin Is a Key Niche Component for Wound Metastasis of Melanoma

et al. 2015

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Low-Fidelity Alternative Dna Repair Carcinogenesis Theory May Interpret Many Cancer Features and Anticancer Strategies

et al. 2016

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We have proposed that the low-fidelity compensatory backup alternative DNA repair pathways drive multistep carcinogenesis. Here, we apply it to interpret the clinical features of cancer, such as mutator phenotype, tissue specificity, age specificity, diverse types of cancers originated from the same type of tissue, cancer susceptibility of patients with DNA repair-defective syndromes, development of cancer only for a selected number of individuals among those that share the same genetic defect, invasion and metastasis. Clinically, the theory predicts that to improve the efficacy of molecular targeted or synthetic lethal therapy, it may be crucial to inhibit the low-fidelity compensatory alternative DNA repair either directly or by blocking the signal transducers of the sustained microenvironmental stress.

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Hypothesis: hematogenous metastatic cancer cells of solid tumors may disguise themselves as memory macrophages for metastasis

Jiang,

2024

Front. Oncol.

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German pathologist Otto Aichel suggested, a century ago, that the cancer cell acquired its metastatic property from a leukocyte via cell-cell fusion. Since then, several revised versions of this theory have been proposed. Most of the proposals attribute the generation of the metastatic cancer cell to the fusion between a primary cancer cell and a macrophage. However, these theories have not addressed several issues, such as dormancy and stem cell-like self-renewal, of the metastatic cancer cell. On the other hand, recent studies have found that, like T- and B-/plasma cells, macrophages can also be categorized into naïve, effector, and memory/trained macrophages. As a memory/trained macrophage can enter dormancy/quiescence, be awakened from the dormancy/quiescence by acquainted primers, and re-populate via stem cell-like self-renewal, we, therefore, further specify that the macrophage fusing with the cancer cell and contributing to metastasis, belongs with the memory/trained macrophage, not other subtypes of macrophages. The current theory can explain many puzzling clinical features of cancer, including the paradoxal effects (recurrence vs. regression) of microbes on tumors, “spontaneous” and Coley’s toxin-induced tumor regression, anticancer activities of β-blockers and anti-inflammatory/anti-immune/antibiotic drugs, oncotaxis, surgery- and trauma-promoted metastasis, and impact of microbiota on tumors. Potential therapeutic strategies, such as Coley’s toxin-like preparations, are proposed. This is the last article of our trilogy on carcinogenesis theories.

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Stimuli-induced Organ-specific Injury Enhancement of Organotropic Metastasis in a Spatiotemporal Regulation

Cited by 3 publications

References 214 publications

Periostin Is a Key Niche Component for Wound Metastasis of Melanoma

Periostin Is a Key Niche Component for Wound Metastasis of Melanoma

Low-Fidelity Alternative Dna Repair Carcinogenesis Theory May Interpret Many Cancer Features and Anticancer Strategies

Hypothesis: hematogenous metastatic cancer cells of solid tumors may disguise themselves as memory macrophages for metastasis

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