Persistent pain accelerates xenograft tumor growth of breast cancer in rat

Li, Jing; Sun, Yunheng; Ding, Gang; Jiang, Feng

doi:10.1016/j.bbrc.2017.12.121

Cited by 8 publications

(6 citation statements)

References 31 publications

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“…For instance, a rat model of breast and bone cancer in which persistent pain coincided with tumor growth, served to reveal a mechanistic link between pain and tumor growth. 46 These studies demonstrated antitumoral effects of drugs with anesthetic (bupivacaine) and analgesic (morphine) properties. 46 These findings were interpreted as indicative of a pro-tumoral role of active peripheral fibers involved in neuropathic pain, which putatively release pro-tumoral factors.…”

Section: Cell Communication Network In Cancermentioning

confidence: 99%

“…46 These studies demonstrated antitumoral effects of drugs with anesthetic (bupivacaine) and analgesic (morphine) properties. 46 These findings were interpreted as indicative of a pro-tumoral role of active peripheral fibers involved in neuropathic pain, which putatively release pro-tumoral factors. Thus, the vicious tumor-promoting circuit is initiated by cancer cells that release axonogenic neurotrophic factors, directly communicating the tumor stroma with the peripheral nervous system (PNS).…”

Section: Cell Communication Network In Cancermentioning

confidence: 99%

“…174,175 Inflammatory mediators lead to the activation of peripheral sensory fibers that, in addition to promoting pain, lead to the release of substance P, a neuropeptide that promotes tumor growth. 46,176 Vasodilation of peri-and intratumor vessels, as well as increased vascular permeability by tumor-derived vasoactive factors contribute to the extravasation of leukocytes to access the tumor and the intravasation of metastatic cells. 177 Inflammation processes induce the accumulation of leukocytes and the release of pain-associated mediators, promoting neuronal plasticity and peripheral innervation.…”

Section: Neuronal Regulation By Tumor-associated Leukocytesmentioning

confidence: 99%

“…Fiber-derived factors Persistent pain (sensorial fibers) stimulate the tumor growth 46 Breast cancer (Walker 256 carcinoma cells). Anesthetic (bupivacaine), analgesic drug (morphine).…”

Section: Sema4f Knock Downmentioning

confidence: 99%

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Tumor-induced neurogenesis and immune evasion as targets of innovative anti-cancer therapies

Cervantes‐Villagrana

Albores-García

Cervantes-Villagrana

et al. 2020

Sig Transduct Target Ther

145

112

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Normal cells are hijacked by cancer cells forming together heterogeneous tumor masses immersed in aberrant communication circuits that facilitate tumor growth and dissemination. Besides the well characterized angiogenic effect of some tumor-derived factors; others, such as BDNF, recruit peripheral nerves and leukocytes. The neurogenic switch, activated by tumor-derived neurotrophins and extracellular vesicles, attracts adjacent peripheral fibers (autonomic/sensorial) and neural progenitor cells. Strikingly, tumor-associated nerve fibers can guide cancer cell dissemination. Moreover, IL-1β, CCL2, PGE 2 , among other chemotactic factors, attract natural immunosuppressive cells, including T regulatory (Tregs), myeloid-derived suppressor cells (MDSCs), and M2 macrophages, to the tumor microenvironment. These leukocytes further exacerbate the aberrant communication circuit releasing factors with neurogenic effect. Furthermore, cancer cells directly evade immune surveillance and the antitumoral actions of natural killer cells by activating immunosuppressive mechanisms elicited by heterophilic complexes, joining cancer and immune cells, formed by PD-L1/PD1 and CD80/CTLA-4 plasma membrane proteins. Altogether, nervous and immune cells, together with fibroblasts, endothelial, and bone-marrow-derived cells, promote tumor growth and enhance the metastatic properties of cancer cells. Inspired by the demonstrated, but restricted, power of anti-angiogenic and immune cell-based therapies, preclinical studies are focusing on strategies aimed to inhibit tumor-induced neurogenesis. Here we discuss the potential of anti-neurogenesis and, considering the interplay between nervous and immune systems, we also focus on anti-immunosuppression-based therapies. Small molecules, antibodies and immune cells are being considered as therapeutic agents, aimed to prevent cancer cell communication with neurons and leukocytes, targeting chemotactic and neurotransmitter signaling pathways linked to perineural invasion and metastasis.

show abstract

Section: Cell Communication Network In Cancermentioning

confidence: 99%

Section: Cell Communication Network In Cancermentioning

confidence: 99%

Section: Neuronal Regulation By Tumor-associated Leukocytesmentioning

confidence: 99%

“…Fiber-derived factors Persistent pain (sensorial fibers) stimulate the tumor growth 46 Breast cancer (Walker 256 carcinoma cells). Anesthetic (bupivacaine), analgesic drug (morphine).…”

Section: Sema4f Knock Downmentioning

confidence: 99%

See 2 more Smart Citations

Tumor-induced neurogenesis and immune evasion as targets of innovative anti-cancer therapies

Cervantes‐Villagrana

Albores-García

Cervantes-Villagrana

et al. 2020

Sig Transduct Target Ther

145

112

View full text Add to dashboard Cite

show abstract

“…17,27,34,33 In cancer patients, pain is commonly associated with tumor growth. 32 Based on the MGS, pain was present in mice from the saline group beginning with the first evaluation on day 8 of the study. The analgesia promoted by 10 mg/kg of morphine reduced allodynia and the MGS scores at 1 h after administration when assessed in a 4T1 breast cancer model in mice.…”

Section: Discussionmentioning

confidence: 99%

Effects of Three Consecutive Days of Morphine or Methadone Administration on Analgesia and Open-Field Activity in Mice with Ehrlich Carcinoma

Rusch

Bovi

Martinelli

et al. 2021

j am assoc lab anim sci

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This study assessed the exploratory behavioral responses in BALB/c mice inoculated with Ehrlich ascitic carcinoma after 3consecutive days of treatment with morphine or methadone. Fifty-three female mice, 60 ± 10 d old, were used. Seven days after intraperitoneal tumor inoculation (2 × 106 cells), the animals were randomized into 7 groups: morphine 5 mg/kg (MO5), morphine 7.5 mg/kg (MO7.5), morphine 10 mg/kg (MO10), methadone 2.85 mg/kg (ME2.85), methadone 4.3 mg/kg (ME4.3), methadone5.7 mg/kg (ME5.7), and 0.9% NaCl (Saline) (n = 7). Drug treatments were administered subcutaneously every 6 h for 3 d. The animals were evaluated for analgesia using the mouse grimace scale (MGS) and for general activity using the open field test. The MGS was performed before tumor inoculation (day 0), on day 7 at 40, 90, 150, 240, and 360 min after drug injection, and on days 8 and 9 at 40, 150, 240, and 360 min after drug injection. The open field test was performed before tumor inoculation(day 0), on day 7 after inoculation at 40, 90, 150, 240, and 360 min after drug injection, and on days 8 and 9 after inoculation at 40, 150, and 360 min after drug injection. MGS results indicated that administration of morphine promoted analgesia for up to 240 min. Conversely, methadone reduced MGS scores only at 40 min. All tested doses promoted a significant dose-dependent increase in the total distance traveled and the average speed, and increase that was markedly pronounced on days 8 and 9 as compared with day 7. The frequencies of rearing and self-grooming decreased significantly after morphine or methadone administration. Despite the difference in analgesia, both drugs increased locomotion and reduced the frequency of rearing and self-grooming as compared with the untreated control animals.

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Dynamic regulation of drug biodistribution by turning tumors into decoys for biomimetic nanoplatform to enhance the chemotherapeutic efficacy of breast cancer with bone metastasis

et al. 2023

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Breast cancer with bone metastasis accounts for serious cancer‐associated pain which significantly reduces the quality of life of affected patients and promotes cancer progression. However, effective treatment using nanomedicine remains a formidable challenge owing to poor drug delivery efficiency to multiple cancer lesions and inappropriate management of cancer‐associated pain. In this study, using engineered macrophage membrane (EMM) and drugs loaded nanoparticle, we constructed a biomimetic nanoplatform (EMM@DJHAD) for the concurrent therapy of bone metastatic breast cancer and associated pain. Tumor tropism inherited from EMM provided the targeting ability for both primary and metastatic lesions. Subsequently, the synergistic combination of decitabine and JTC801 boosted the lytic and inflammatory responses accompanied by a tumoricidal effect, which transformed the tumor into an ideal decoy for EMM, resulting in prolonged troop migration toward tumors. EMM@DJHAD exerted significant effects on tumor suppression and a pronounced analgesic effect by inhibiting µ‐opioid receptors in bone metastasis mouse models. Moreover, the nanoplatform significantly reduced the severe toxicity induced by chemotherapy agents. Overall, this biomimetic nanoplatform with good biocompatibility may be used for the effective treatment of breast cancer with bone metastasis.

show abstract

Persistent pain accelerates xenograft tumor growth of breast cancer in rat

Cited by 8 publications

References 31 publications

Tumor-induced neurogenesis and immune evasion as targets of innovative anti-cancer therapies

Tumor-induced neurogenesis and immune evasion as targets of innovative anti-cancer therapies

Effects of Three Consecutive Days of Morphine or Methadone Administration on Analgesia and Open-Field Activity in Mice with Ehrlich Carcinoma

Dynamic regulation of drug biodistribution by turning tumors into decoys for biomimetic nanoplatform to enhance the chemotherapeutic efficacy of breast cancer with bone metastasis

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