Shell remains are common cultural relics recovered from the late Paleolithic to the historical-age sites in China. Archaeological evidence shows that the number of perforated shells gradually increased at the transition from the Paleolithic to Neolithic age, a time period that coincides with the beginning of farming activities. Usage traces and plant residues from prehistoric perforated shells are often used to interpret tool function. In this study, we analyzed use-wear traces and recovered ancient starches and phytoliths from both the ventral and dorsal margin of twelve perforated shells from the Xianrendong and Diaotonghuan sites (30,000–12,000 cal. Y BP). These sites are well-known for the earliest pottery and the earliest cultivated rice micro-remains in the world. We found that: (1) all the twelve shells had scars and use wear, and that these use traces occurred on the edges of the shells; (2) an assemblage of 83 identifiable starch grains were recovered from the twelve perforated shells, including remains of starches from acorns, Panicoideae and the tribe Triticeae, tubers and roots; (3) only six phytoliths from the stems and leaves of grass taxa including Panicoideae and Bambusoideae were recovered from four shells. The meta-analysis of the use-wear and plant micro-remain analysis indicate that the functions of perforated shells were nearly identical from the late Paleolithic to early Neolithic periods. These functions include processing, harvesting or cutting grasses from the Panicoideae, Bambusoideae, and the tribe Triticeae, processing acorns or/and their starchy products, in addition to digging up and scraping tubers and roots. The digging and scraping of tubers and roots increased in intensity with the increase in rice cultivation during the period between 20,000 and 12,000 cal. Y BP.
Hadron therapy with protons and carbon ions is widely attracting interest as a potential competitor of conventional photon radiotherapy. Exquisite dose distribution of charged particles allows for a higher local control of the tumor and lower probability of damage to nearby healthy tissues. Heavy ions have presumed biological advantages rising from their high-linear energy transfer (LET) characteristics, including greater cell-killing effectiveness and reduced heterogeneity dependence of radiation response. Although these advantages are clear and supported by data, only 18.0% of proton and carbon ion radiotherapy (CIRT) facilities in Europe are treating breast cancers. This review summarizes the physical and radiobiological properties of charged particles, clinical use of particle beam for breast cancer, and suggested approaches to overcome technical and financial challenges.
Cancer cells maintain a high level of aerobic glycolysis (the Warburg effect), which is associated with their rapid proliferation. Many studies have reported that the suppression of glycolysis and activation of oxidative phosphorylation can repress the growth of cancer cells through regulation of key regulators. Whether Warburg effect of cancer cells could be switched by some other environmental stimulus? Herein, we report an interesting phenomenon in which cells alternated between glycolysis and mitochondrial respiration depending on the type of radiation they were exposed to. We observed enhanced glycolysis and mitochondrial respiration in HeLa cells exposed to 2-Gy X-ray and 2-Gy carbon ion radiation, respectively. This discovery may provide novel insights for tumor therapy.
The occurrence of distant tumor metastases is a major barrier in non-small cell lung cancer (NSCLC) therapy, and seriously affects clinical treatment and patient prognosis. Recently, long non-coding RNAs (lncRNAs) have been demonstrated to be crucial regulators of metastasis in lung cancer. The aim of this study was to reveal the underlying mechanisms of a novel lncRNA LNC CRYBG3 in regulating NSCLC metastasis. Experimental results showed that LNC CRYBG3 was upregulated in NSCLC cells compared with normal tissue cells, and its level was involved in these cells’ metastatic ability. Exogenously overexpressed LNC CRYBG3 increased the metastatic ability and the protein expression level of the metastasis-associated proteins Snail and Vimentin in low metastatic lung cancer HCC827 cell line. In addition, LNC CRYBG3 contributed to HCC827 cell metastasis in vivo. Mechanistically, LNC CRYBG3 could directly combine with eEF1A1 and promote it to move into the nucleus to enhance the transcription of MDM2. Overexpressed MDM2 combined with MDM2 binding protein (MTBP) to reduce the binding of MTBP with ACTN4 and consequently increased cell migration mediated by ACTN4. In conclusion, the LNC CRYBG3/eEF1A1/MDM2/MTBP axis is a novel signaling pathway regulating tumor metastasis and may be a potential therapeutic target for NSCLC treatment.
Up to now, more than 1048 human miRNAs have been identified. However, the recognition of new human miRNAs is becoming more and more difficult. Based on the hypothesis that the expression of some miRNAs can be induced by ionizing radiation, total RNAs of HeLa cells were isolated 1 h after exposure to 2 Gy of X-rays, and total small RNAs were enriched and sequenced by PAGE and Solexa technology, respectively. As a result, 421 kinds of known miRNAs and 337 kinds of unknown sequences were identified, among which 10 novel miRNAs were characterized by bioinformatic approach and verified by qRT-PCR. Finally, putative targets of these miRNAs were predicted by TargetScan software and compared with known proteins down-regulated by radiation. It was confirmed that some of the targets of these novel miRNAs were radiation-related proteins. These results imply that these 10 novel miRNAs are radiation-related miRNAs. This study reveals a new way to find novel miRNAs.
The work is to investigate effect of AdCMV-p53 gene transfer on the radiosensitivity of tumor cells. HepG2 (wtp53), Hela (wtp53, low level wtp53 expression) and HT-29 (mtp53, mtp53 over-expression) cells exposed to 0, 0.25, 0.5, 1.0, 1.5 and 2.0Gy were infected with AdCMV-GFP, a replication deficient recombinant adenoviral vector containing a CMV promoter and green fluorescent protein, or AdCMV-p53, a replication deficient recombinant ade-noviral vector containing a CMV promoter and carrying human wild-type p53 gene. Survival fraction of the cells was determined by clonogenic assay. Survival curves were generated by linear quadratic model. The results showed that AdCMV-p53 infection could significantly promote the radiosensitivity of tumor cells. There is a relationship between the effect of AdCMV-p53 infection and the cellular intrinsic p53 status.
Our recent study showed that quiescent G0 cells are more resistant to ionizing radiation than G1 cells; however, the underlying mechanism for this increased radioresistance is unknown. Based on the relatively lower DNA damage induced in G0 cells, we hypothesize that these cells are exposed to less oxidative stress during exposure. As a catalytic subunit of NADPH oxidase, Ras-related C3 botulinum toxin substrate 2 (RAC2) may be involved in the cellular response to ionizing radiation. Here, we show that RAC2 was expressed at low levels in G0 cells but increased substantially in G1 cells. Relative to G1 cells, the total antioxidant capacity in G0 phase cells increased upon exposure to X-ray radiation, whereas the intracellular concentration of ROS and malondialdehyde increased only slightly. The induction of DNA single- and double-stranded breaks in G1 cells by X-ray radiation was inhibited by knockdown of RAC2. P38 MAPK interaction with RAC2 resulted in a decrease of functional RAC2. Increased phosphorylation of P38 MAPK in G0 cells also increased cellular radioresistance; however, excessive production of ROS caused P38 MAPK dephosphorylation. P38 MAPK, phosphorylated P38 MAPK, and RAC2 regulated in mutual feedback and negative feedback regulatory pathways, resulting in the radioresistance of G0 cells.
Long noncoding RNAs (lncRNAs) are usually associated with tumor development and progression and some of them are dysregulated in various human cancers.The mechanisms underlying their dysregulation are worth further study.Here, we demonstrate that the expression level of LNC CRYBG3 is correlated with 1501 aberrantly expressed proteins in A549 cells (non-small cell lung cancer (NSCLC) cells).LNC CRYBG3 overexpression results in M phase arrest and promoted cell death, whereas LNC CRYBG3 knockdown did not elicit the opposite effects.The overexpression of LNC CRYBG3 inhibits cell proliferation both in vitro and in vivo.Moreover, it upregulates the expression of cyclin B1 and the phosphorylation of H3, whereas it inhibited the expression of cyclin-dependent kinase 6 and cyclin D1.Taken together, these findings suggest that LNC CRYBG3 regulates the cell cycle process of A549 cells, suggesting its potential application for the treatment of this disease.
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