Association of the 24-hour movement behaviours composition with workers’ chronic musculoskeletal pain

by Aino Kitayama, Yu-Tai Liu, Ai Shibata, Sayaka Kurosawa, Koichiro Oka

Background

Chronic musculoskeletal pain is a significant symptom among workers. 24-hour movement behaviours comprising sleep, sedentary behaviour, light-intensity physical activity, and moderate-to-vigorous-intensity physical activity are associated factors. However, the relationships between these behaviours and workers’ chronic musculoskeletal pain, considering the interrelationship between the behaviours, are still unclear. This study aimed to investigate the associations of 24-hour movement behaviours with workers’ low-back and neck/shoulder pain.

Methods

In 2023, cross-sectional survey was conducted targeting adults who registered for a Japanese Internet survey system. Time for 24-hour movement behaviours and other demographic characteristics (age, gender, marital status, education, household income, height, weight, smoking, alcohol, chronic disease, work hours, and job activity) were self-reported. The intensity of low-back and neck/shoulder pain was evaluated using the numerical rating scale and a score of ≥4 was considered as moderate-to-severe pain. Compositional logistic regression and isotemporal substitution were performed to examine the associations of 24-hour movement behaviours and time reallocations between the behaviours with moderate-to-severe low-back and neck/shoulder pain, adjusted for all the demographic variables.

Results

1,665 full-time workers (women: 35.8%, mean age: 42.1 ± 10.2 years) were analysed. Increased sleep and decreased light-intensity or moderate-to-vigorous-intensity physical activity were associated with lower odds of moderate-to-severe low-back (adjusted odds ratio [AOR] = 0.54, 95% confidence interval [CI] = 0.40–0.72; 1.45, 1.25–1.69; 1.17, 1.06–1.30, respectively) and neck/shoulder pain (AOR = 0.60, 95% CI = 0.45–0.80; 1.37, 1.19–1.60; 1.12, 1.01–1.24, respectively). Reallocating sleep from the other behaviours was associated with decreased probabilities of low-back and neck/shoulder pain, whereas replacing sedentary behaviour or light-intensity physical activity with more intense activity was associated with increased probabilities. However, the results of moderate-to-vigorous-intensity physical activity reallocation were no longer significant when restricted to complete cases.

Conclusions

Considering the interrelationship of 24-hour movement behaviours, sleep was favourably associated with workers’ low-back and neck/shoulder pain.

EpCAM silencing suppresses aggressive phenotypes and induces partial redifferentiation in anaplastic thyroid cancer cells

by Teruo Nakamura, Tomohiro Shibata, Ken-ichi Ito

Anaplastic thyroid cancer (ATC) is a rare but highly aggressive malignancy with a dismal prognosis. Although recent advances in targeted therapies have modestly improved survival, the molecular mechanisms driving ATC progression remain incompletely elucidated. Epithelial cell adhesion molecule (EpCAM), a multifunctional cell-surface protein, is implicated in proliferation, migration, and stemness in various cancers. However, its role in thyroid cancer progression remains unclear. In this study, we investigated the function of EpCAM in thyroid cancer cell lines of varying differentiation status. EpCAM expression was significantly elevated in ATC cell lines compared with differentiated thyroid cancer (DTC) lines. EpCAM knockdown by siRNA suppressed proliferation, adhesion, motility, and invasion in ATC cells, but had minimal effects on DTC cells. Morphological analyses revealed that EpCAM silencing induced differentiation features, including follicle-like structure formation and increased expression of thyroid differentiation markers such as thyroglobulin and PAX8 in ATC cells. Furthermore, EpCAM inhibition decreased mesenchymal marker expression, reduced filopodia formation, and suppressed extravasation of cancer cells into the lung in an in vivo mouse model. Mechanistically, EpCAM knockdown attenuated epithelial–mesenchymal transition (EMT)-related pathways but did not affect major proliferation signaling cascades in ATC cells. These findings suggest that EpCAM promotes dedifferentiation and metastatic potential in ATC through EMT modulation. Our results provide new insights into the role of EpCAM in thyroid cancer biology and highlight its potential as a therapeutic target in ATC. Further studies are warranted to elucidate the mechanisms linking EpCAM to anaplastic transformation and to explore the therapeutic efficacy of EpCAM-targeting strategies in aggressive thyroid cancers.