Membrane-bound TNF mediates microtubule-targeting chemotherapeutics-induced cancer cytolysis via juxtacrine inter-cancer-cell death signaling
CELL DEATH AND DIFFERENTIATION
Authors: Zhang, Jing; Yang, Yu; Zhou, Shenao; He, Xueyan; Cao, Xuan; Wu, Chenlu; Hu, Hong; Qin, Jie; Wei, Gang; Wang, Huayi; Liu, Suling; Sun, Liming
Microtubule-targeting agents (MTAs) are a class of most widely used chemotherapeutics and their mechanism of action has long been assumed to be mitotic arrest of rapidly dividing tumor cells. In contrast to such notion, here we show-in many cancer cell types-MTAs function by triggering membrane TNF (memTNF)-mediated cancer-cell-to-cancer-cell killing, which differs greatly from other non-MTA cell-cycle-arresting agents. The killing is through programmed cell death (PCD), either in way of necroptosis when RIP3 kinase is expressed, or of apoptosis in its absence. Mechanistically, MTAs induce memTNF transcription via the JNK-cJun signaling pathway. With respect to chemotherapy regimens, our results establish that memTNF-mediated killing is significantly augmented by IAP antagonists (Smac mimetics) in a broad spectrum of cancer types, and with their effects most prominently manifested in patient-derived xenograft (PDX) models in which cell-cell contacts are highly reminiscent of human tumors. Therefore, our finding indicates that memTNF can serve as a marker for patient responsiveness, and Smac mimetics will be effective adjuvants for MTA chemotherapeutics. The present study reframes our fundamental biochemical understanding of how MTAs take advantage of the natural tight contact of tumor cells and utilize memTNF-mediated death signaling to induce the entire tumor regression.
Phytoremediation Mechanisms in Air Pollution Control: a Review
WATER AIR AND SOIL POLLUTION
Authors: Lee, Bernice Xin Yi; Hadibarata, Tony; Yuniarto, Adhi
Air pollutants originated from natural and anthropogenic sources and able to bio-magnify and bio-accumulate in the trophic levels, thus increase toxicity in the food chain. Various air pollutants (particulate matters (PMs), volatile organic compounds (VOCs), inorganic air pollutants (IAP), persistent organic pollutants (POPs), heavy metals, and black carbon) resulted in adverse effects on environmental and human health after prolonged exposure. These airborne particles can travel in gaseous form for long distance and deteriorate the air quality of downstream areas. Air pollution abatement can be implemented by reducing emissions at source and purifying pollutants with remediation techniques. However, air pollution remained as the dominant issue to cause burden in human and ecosystem well-being. Due to drawbacks like expensive, high maintenance, and likelihood for pollutants' reemission, existing conventional remediation technologies is insufficient for air pollutants mitigation. Phytoremediation enters the picture of air pollution control as a cost-effective, energy-saving, and environmental-friendly technology in remediating air pollutants. In phytoremediation, plant organs and associating microbes in the phyllosphere and rhizosphere interacted with each other to remediate air pollutants. Phytoremediation of air pollutants involves the rhizosphere of plants as pollutants may deposit in the soil during leaf fall and precipitation. Additionally, the phytoremediation mechanisms involve phytoextraction, phytovolatilization, phytodegradation, phytostabilization, rhizodegradation, and rhizofiltration. A brief overview of phytoremediation mechanisms for each air pollutants is presented. In short, the benefits of phytoremediation and its associated gaps in air pollution control are described.